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Phlegmons are unencapsulated collections of inflammation that track along soft tissues in various parts of the human body. These soft-tissue lesions are uncommon in the lower extremities and can be difficult to identify and treat. This article presents a case of a plantar foot phlegmon in a nondiabetic patient that was recalcitrant to debridement and antibiotics. The patient's aseptic phlegmon completely resolved with surgical debridement and iodoform packing. This case report demonstrates the role of advanced imaging in the diagnosis of lower-extremity phlegmons and the importance of thorough surgical debridement and packing for successful resolution.

Invasive, nuisance aquatic species such as Eurasian watermilfoil (Myriophyllum spicatum) are rapidly spreading across the United States. One common active ingredient used to control this invasive species is 2,4-Dichlorophenoxyacetic acid (2,4-D). Application of 2,4-D to aquatic environments typically occurs while many freshwater fish are spawning and due to 2,4-D stability in aquatic environments, many non-target species experience prolonged exposure throughout embryogenesis and larval development. The impacts of 2,4-D exposure on phylogenetically distant fish species is poorly understood. Herein, we investigated the impacts of the 2,4-D commercial herbicide DMA4®IVM on nine freshwater fish species from six different families (four orders) at different points during ontogeny. Each species was exposed to ecologically relevant concentrations of a commercial 2,4-D herbicide (0.05, 0.50, and 2.00 ppm or mg/L 2,4-D a. e.), and effects on morphology, survival, and growth were evaluated. Our results demonstrate that exposure of embryonic and larval fish to ecologically relevant concentrations of a commercial 2,4-D herbicide reduced survival in early developmental stages of six freshwater species that spanned five phylogenetic families and three phylogenetic orders; however, sensitivity to 2,4-D exposure did not show correlation with phylogenetic proximity. Altogether, our results indicate that the use of 2,4-D herbicides in aquatic ecosystems at current recommended concentrations (≤2 ppm whole-lake treatment) could present risk to multiple freshwater fish species survival during early development., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Introduction: It is well established that work stress is a major economic burden not only in lost work productivity but also in increased health care utilization and costs. However, there is little research into effective treatment models for work stress., Objective: To retrospectively examine the effectiveness of a psychiatric pilot quality improvement program in improving the return-to-work rate in patients in a health maintenance organization who had work stress and took medical leave from work., Methods: A health maintenance organization's Department of Psychiatry developed a pilot quality improvement program that reviewed a new program of group psychotherapy and specialty mental health treatment targeting patients who self-identified as having work stress and who requested medical leave from work. The retrospective data were collected from the electronic medical record., Results: Of the 166 patients who participated in the Work Recovery Group program, 141 (85%) returned to work and did not have any days off after the Work Recovery Group within the 11-month analysis. Involvement in the group also was associated with improvement in self-reported symptom severity, with a 4.5-point decrease in the average score on the Adult Outcomes Questionnaire about depression and anxiety., Discussion: This is the first known treatment program from a health maintenance organization to provide data on return-to-work outcomes. By providing specialty mental health treatment and getting patients back to work more quickly, this program has potential to reduce mental health service utilization. These results show promise for program expansion and have broader implications for health care organizations and employers.

Water-soluble factors associated with walleye Sander vitreus predation on either yellow perch Perca flavescens or fathead minnows Pimephales promelas markedly increased the growth rate of P. flavescens. The findings suggest that P. flavescens possess an inducible growth-promoting mechanism regulated by water-born chemicals. It may be possible to increase the growth rate of farm-raised P. flavescens by manipulating this system., (© 2017 The Fisheries Society of the British Isles.)

High concentrations (300 ng/L) of androstenedione (A4) were identified in snowmelt runoff from fields fertilized with manure from livestock feeding operations in Wisconsin, USA. In fishes, A4 is an active androgen and substrate for biosynthesis of functional androgens (e.g., testosterone and 11-ketotestosterone) and estrogens (e.g., estradiol-17β). Thus, A4 has the potential to be a powerful endocrine disruptor. This hypothesis was tested by exposing reproductively mature fathead minnows to 0.0 ng/L, 4.5 ng/L, 74 ng/L, and 700 ng/L A4 for 26 d in a flow-through system. Various reproductive endpoints were measured including fecundity, fertilization success, secondary sexual characteristics, gonadosomatic index (GSI), and hepatic vitellogenin messenger RNA (mRNA) expression. In addition, fertilized embryos from the reproduction assay were used in an embryonic development assay to assess A4 effects on development and hatchability. In males, A4 significantly increased Vtg mRNA expression (estrogenic effect), significantly reduced GSI, and had no effect on tubercle expression (p = 0.067). In females, A4 induced tubercle development (androgenic effect) with no effects on GSI. Fecundity was not significantly impacted. Exposure to A4 had no effect on fertilization, embryonic development, or hatchability. These data indicate that exogenous A4, at environmentally relevant concentrations, can significantly modulate the reproductive physiology of the fathead minnows in a sex-specific manner and that A4 should be monitored as an endocrine disruptor., (© 2015 SETAC.)

High concentrations (375 ng/L) of the steroid hormone progesterone (P4) were measured in snowmelt runoff associated with large livestock-feeding operations in Wisconsin. To gain insight into the potential endocrine-disrupting effects of P4 in fish, experiments were conducted to evaluate the effects of short-term exposure to environmentally relevant concentrations of P4 on reproduction and embryonic development in the fathead minnow (Pimephales promelas). For the reproduction assay, groups of reproductively mature fish were exposed for 21 d to nominal concentrations of 0, 10, 100, and 1,000 ng/L P4 in a flow-through system, and various key reproductive endpoints (e.g., egg number, fertilization success) were quantified throughout the exposure period. The embryonic development assay consisted of incubating fathead minnow eggs in static culture to quantify the effects of P4 on early development and hatching success. Progesterone caused dose-dependent decreases in fecundity and fertility and significantly reduced gonadosomatic index and vitellogenin gene expression in females. There were no effects of P4 on early embryonic development or hatching success. Progesterone may be a significant endocrine-disrupting chemical in fish., (Copyright © 2012 SETAC.)

The steroid hormone progesterone (P4) is found at relatively high concentrations (∼300 ng/L) in association with concentrated animal feeding operations (CAFOs). In an effort to better understand the potential endocrine disrupting effects of P4 in male fish, computer assisted sperm analysis (CASA) was used to evaluate the effects of this steroid on sperm motility in the fathead minnow (Pimephales promelas). The rationale for focusing on sperm motility is that certain progestins have been shown to bind to surface membrane receptors on fish spermatozoa and increase sperm swimming velocity. It was hypothesized, therefore, that sperm swimming velocity might be a useful indicator of progestin exposure in fish. Adult male fathead minnows (ages 6-12 months) were exposed to environmentally relevant doses of P4, both longer-term (1 week, in vivo exposure) and short-term (minutes, in vitro exposure). Sperm were then video recorded and analyzed by CASA. When fathead minnows were continuously exposed for 1 week to low levels of progesterone in vivo there was a significant dose-dependent reduction in sperm motility. There was no effect of short-term P4 exposure on fathead minnow sperm swimming characteristics. Additional research is required to elucidate the mechanism by which progesterone alters sperm swimming in the fathead minnow. With further validation, the fathead minnow sperm motility assay may be a useful tool to rapidly screen for endocrine disrupting chemicals in the aquatic environment., (Copyright © 2011 Elsevier B.V. All rights reserved.)

In vitro experiments were conducted to test the hypothesis that 17alpha,20beta-dihydroxy-4-prengnen-3-one (17,20-P) regulates cortisol metabolism in Pacific salmon. In both rainbow trout and coho salmon, cortisol metabolism was significantly higher in the kidney compared to the liver. The rainbow trout kidney converted cortisol primarily into an unidentified water-soluble metabolite with a molecular mass of 354. The coho salmon kidney converted cortisol primarily into cortisol-21-sulfate. High physiological concentrations of 17,20-P had no effect on cortisol metabolism by the rainbow trout kidney, but almost completely inhibited the production of cortisol-21-sulfate by the coho salmon kidney. This was accompanied by a coincident increase in the production several neutral cortisol metabolites, including cortisone. Cortisone was also found to inhibit renal sulfotransferase (SULT) activity suggesting that there could be a local positive feedback mechanism initiated by the rise in 17,20-P that quickly reduces SULT activity as follows: the pre-spawning rise in 17,20-P inhibits SULT, cortisol is metabolized to cortisone instead of cortisol-21-sulfate, cortisone further inhibits SULT, more cortisone is produced, and so on. If SULT normally acts as a gatekeeper enzyme to protect the cell from cortisol excess, this mechanism would rapidly remove enzymatic protection and expose tissues to high local concentrations of cortisol. In addition, the inhibition of peripheral cortisol metabolism by 17,20-P could increase circulating concentrations of the corticosteroid. These events could be a part of the mechanism that leads to the symptoms of cortisol excess associated with the post-spawning mortality of semelparous Pacific salmon.

The medical literature presents diabetic sensory polyneuropathy (DSPN) as an axonal length-dependent symmetric pathology producing a stocking-like pattern of anesthesia in the lower extremities. This has been based on anecdotal reports. Objective research has shown that damage may not occur in a purely length-dependent manner. A stocking distribution of sensory loss is atypical, and plantar sensory loss predominates. A single-blinded, age-matched, control/experimental study was performed of the symmetry of nerve damage in developing DSPN. Control (n = 46) and experimental (n = 83) subjects were examined. The patterns of sensory loss and the severity of axonal damage were evaluated. The right/left symmetry of pathology was recorded for each individual. Although there was not a stocking pattern of anesthesia found in developing DSPN, the pattern and severity of anesthesia were found to be generally symmetric. The severity of sensory impairment was symmetric at the dorsal foot (93%), lateral foot (95%), and plantar foot (69%). The most predominant site of sensory impairment was also symmetric (81%). This argues against a purely metabolic etiology for axonal damage. An anatomic component is implied. Further research will need to include examination of the unique physical characteristics of predominantly affected nerves.

The medical literature presents diabetic sensory polyneuropathy as a length-dependent process producing a stocking distribution of sensory loss in the lower extremities. If a purely length-dependent etiology for diabetic sensory polyneuropathy were true, then a validated comparison of sensory loss at any equidistant site about the forefoot will reveal findings consistent with the accepted stocking pattern of anesthesia. A single-blinded, age-matched, control/experimental study is made into the frequency of apparent purely length-dependent A-beta fiber pathology in developing diabetic sensory polyneuropathy. Control (n = 46) and experimental (n = 83) central US subjects are examined with a subjective neuropathy screening questionnaire, vibratory threshold, and single-point pressure threshold testing. There is a plantar predominant pattern (61.5%) of sensory loss in developing diabetic sensory polyneuropathy, even after adjusting for sensitivity differences between different areas of the foot. A typical stocking pattern of sensory loss was not found. Although axonal pathology is length dependent, it is not apparently a purely length-dependent process. Therefore, a purely metabolic explanation for sensory loss is unlikely. In addition, an anatomic component for A-beta fiber pathology is implied by this study.

Experiments were conducted to (1) elucidate the biochemical pathways of E2 metabolism in the lake trout (Salvelinus namaycush) kidney and liver, and (2) test the hypothesis that specific xenobiotics and endogenous steroids inhibit E2 metabolism by these tissues. Kidney and liver tissue fragments from immature lake trout were incubated in vitro in the presence of radiolabelled E2 plus various xenobiotics or steroids. E2 metabolites were identified by liquid chromatography/mass spectroscopy, and quantified by liquid scintillation spectroscopy. A major metabolite produced by both tissues was an unidentified hydroxylated estrogen metabolite (E2-OH) with a molecular mass of 288 that was not estriol (16-OH-E2), but possibly 7alpha-OH-E2 or 2-OH-E2 (catecholestrogen). Both tissues also produced estradiol-17-glucuronide (E2-17-G), estradiol-17-sulfate (E2-17-S), and estradiol-3-glucuronide (E2-3-G). Compared to the kidney, the liver produced half the amount of conjugated metabolites, but twofold more E2-OH. The following xenobiotics (at a concentration of 100 microM) inhibited the production of water-soluble (i.e., conjugated) E2 metabolites by both the kidney and liver: 4,4'-(OH)2-3,3',5,5'- tetrachlorobiphenyl (4,4'-OH-TCB), bisphenol A (BPA), tetrabromobisphenol A (TB-BPA), tetrachlorobisphenol A (TC-BPA), tribromophenol (TBP), trichlorophenol (TCP), and pentachlorophenol (PCP). The alkylphenols, 4-n-nonylphenol (NP), and 4-octylphenol (OP), and 2,2',4,4'-tetrabromodiphenyl ether (TBDE) had no significant effect on E2 metabolism by either tissue. Testosterone and 17alpha,20beta-dihydroxy-4-pregnen-3-one inhibited the production of conjugated E2 metabolites by both the kidney and liver. Cortisol and 11-ketotestosterone inhibited E2 metabolism by the liver only. The median inhibitory concentrations (IC50) for 4,4'-OH-TCB ranged from 7-32 microM in the kidney and 0.6-1.6 microM in the liver. For BPA, IC50's ranged from 40-108 microM in the kidney and 11-18 microM in the liver. Low doses (0.1 microM) of 4,4'-OH-TCB and BPA significantly increased estrogen metabolism in the kidney. The results suggest that certain estrogenic xenobiotics and endogenous steroids may inhibit the phase II conjugation of E2 by the kidney and liver of lake trout, and some of the known biological effects of these compounds are likely mediated, at least partially, by this mechanism of action.

Physiological levels of 17alpha,20beta-dihydroxy-4-pregnen-3-one (17, 20-P) stimulated time- and dose-dependent increases in cortisol production by rainbow trout (Oncorhynchus mykiss) interrenal tissue cultured in vitro. Significant stimulation occurred in response to 100, 300, and 1000 ng/ml of 17,20-P. Lower doses were ineffective. Elevated cortisol levels were observed 1 hr after addition of 300 ng/ml 17,20-P. No additive or synergistic interaction was evident between human adrenocorticotropin fragment 1-24 (ACTH1-24) and 17, 20-P in stimulating cortisol secretion, although 300 ng/ml 17,20-P could further enhance cortisol production above levels already stimulated by 300 ng/ml ACTH. 17alpha, 20alpha-dihydroxy-4-pregnen-3-one also stimulated cortisol secretion, but was only half as effective as 17,20-P. Estradiol-17beta, testosterone, and 11-ketotestosterone had no effect on cortisol secretion. Inhibitors of mRNA and protein synthesis had no effect on 17,20-P-stimulated cortisol production. Radiotracer studies demonstrated that the bioconversion of 17,20-P to cortisol could fully account for the cortisol produced by the interrenal in response to 17,20-P and demonstrated that rainbow trout interrenal cells contain an active 20beta-hydroxysteroid dehydrogenase. These data suggest that 17,20-P may be a regulator of cortisol production during the periovulatory period in salmonid fishes.

Interrenal tissue from embryonic and larval rainbow trout (Oncorhynchus mykiss) was cultured in vitro and exposed to various doses of adrenocorticotropin (ACTH) to document the ontogeny of interrenal responsiveness to tropic stimulation. Resting and acute stress-induced changes in whole-body cortisol levels in vivo were also measured to determine if the corticosteroid stress response first develops with the onset of interrenal responsiveness to ACTH. No evidence was found that the hypothalamic-pituitary-interrenal (HPI) axis of rainbow trout is transiently activated prior to hatching. In vivo, a corticosteroid stress response was first observed 2 weeks after hatching, and stress-induced cortisol levels (at 1 hr poststress) were significantly higher 3 weeks after hatching than they were at 2 or 4 weeks after hatching. In contrast, cultured interrenal tissue produced significant levels of cortisol in response to ACTH at the time of hatching, and in vitro cortisol production by the interrenal increased significantly between 3 and 4 weeks after hatching. Interrenal sensitivity to ACTH did not change appreciably with development. We conclude that (1) the final maturation of the corticosteroid stress response in rainbow trout occurs at the level of the brain and/or sensory inputs and not at the level of the interrenal cell; (2) negative feedback mechanisms within the HPI axis develop 3 to 4 weeks after hatching; and (3) the period between 3 and 4 weeks after hatching may be homologous to the stress hyporesponsive period after birth in mammals and thus could be a stage when environmental influences can permanently alter the development of the corticosteroid stress response in rainbow trout.

The ontogeny of the interrenal stress response in rainbow trout was characterized by measuring resting and acute-stress-induced changes in whole-body cortisol levels in embryos and larvae at different early developmental stages. In Experiment 1, resting cortisol levels averaged 6.0 ng/g in newly fertilized eggs, fell to less than 0.3 ng/g by the time of hatching at Week 4 (incubation at 10 degrees), and increased to 1.4 ng/g by Week 5. Cortisol levels did not change in response to acute stress in 3-, 4-, or 5-week-old fish. In Experiment 2, resting cortisol averaged 1.4 ng/g in newly fertilized eggs, fell to less than 0.03 ng/g by Week 2, and then steadily increased between Weeks 3 and 6 to a peak of 4.8 ng/g before falling to 1.2 ng/g by Week 7. Cortisol levels did not change in response to acute stress in 3-, 4-, or 5-week-old fish. Six-week-old fish showed a 2.3-fold increase in cortisol levels at 1 hr poststress, indicating that the hypothalamic-pituitary-interrenal axis first develops responsiveness to stress 2 weeks after hatching and 1 week before the onset of exogenous feeding. The stress hyporesponsive period after hatching in rainbow trout may be homologous to the 2-week stress hyporesponsive period after birth in rodents, the function of which may be to maintain low, constant corticosteroid levels during a critical developmental period when these steroids can have permanent effects on neural organization. As suggested for mammals, this period may be a time when rainbow trout are particularly vulnerable to environmental effects on their subsequent development.

The annual reproductive cycle of walleye (Stizostedion vitreum) was characterized by documenting changes in gonadal development and serum levels of estradiol-17β (E2), testosterone (T), 17α,20β-dihydroxy-4-pregnen-3-one (17,20-P), and 11-ketotestosterone (11-KT) in wild fish captured from upper midwestern lakes and rivers throughout the year. Fish from the populations used in this study spawn annually in early- to mid-April. Walleye showed group synchronous ovarian development with exogenous vitellogenesis beginning in autumn. Oocyte diameters increased rapidly from ∼ 200 μm in October to ∼ 1,000 μm in November, and reached a maximum of 1,500 μm just prior to spawning. Changes in gonadosomatic indices (GSIs) paralleled changes in oocyte diameters. Serum E2 levels in females increased rapidly from low values in October (< 0.1 ng ml(-1)) to peak levels of 3.7 ng ml(-1) in November, coinciding with the period of the most rapid ovarian growth. Subsequently, E2 levels decreased from December through spawning. Serum T levels exhibited a bimodal pattern, increasing to 1.6 ng ml(-1) in November, and peaking again at 3.3 ng ml(-1) just prior to spawning. We detected 11-KT in the serum of some females at concentrations up to 5.6 ng ml(-1), but no seasonal pattern was apparent. In this study (unlike our results in a related study) 17,20-P was not detected. In males, differentiation of spermatogonia began in late August, and by January the testes were filled (> 95% of germ cells) with spermatozoa. Mature spermatozoa could be expressed from males from January through April. GSIs ranged from 0.2% (post-spawn) to 3.2% (pre-spawn). Serum T levels rose from undetectable levels in post-spawn males to 1.6 ng ml(-1) by November, remained elevated throughout the winter, and peaked at 2.8 ng ml(-1) I prior to spawning. Levels of 11-KT in males remained low (< 10 ng ml(-1), from post-spawning through January, then increased significantly by March and peaked just prior to spawning at 39.7 ng ml(-1). Our results indicate that vitellogenesis and spermatogenesis are complete or nearly so, in walleye by early winter, and suggest that it may be possible to induce spawning in this species several months prior to the normal spawning season by subjecting fish to relatively simple environmental and hormonal treatments.

Using shark (Squalus acanthias) testicular microsomes and [3H]progesterone ([3H]P) and [3H]17 alpha-hydroxyprogesterone ([3H]17 alpha-P) as substrates, two major products of 21-hydroxylase action were identified; respectively, 21-hydroxy-4-pregnen-3-one (11-deoxycorticosterone, DOC) and 17 alpha,21-dihydroxy-4-pregnen-3-one (11-deoxycortisol,S). Additional products of 17 alpha-hydroxylase/C-17,20-lyase action were detected: 17 alpha-hydroxyprogesterone (17 alpha P), testosterone (T), and androstenedione (AE). When microsomes derived from tissues in premeiotic (PrM), meiotic (M), and postmeiotic (PoM) stages of spermatogenesis were compared, maturation-related increases were observed with both 21-hydroxylase (3- to 20-fold) and 17 alpha-hydroxylase (2- to 6-fold). With [3H]P as tracer, the half-maximal substrate concentrations (Km = 0.2-1.0 microM) and maximal reaction velocities (Vmax = 9-25 pmol/mg protein/min) were similar for both enzymes when assayed in the same preparation, suggesting they compete for available substrate. Also, the presence of 1- or 10-fold molar excess radioinert DOC reduced conversion of [3H]P to 17 alpha-hydroxylated products. [3H]DOC itself was a substrate of 17 alpha-hydroxylation but not C-17,20-lyase action. Expression of 21-hydroxylase and 17 alpha-hydroxylase activities in cultured spermatocysts (intact germ cell/Sertoli cell units) was confirmed by detection of immunoreactive 17 alpha,20 beta,21-trihydroxy-4-pregnen-3-one (20 beta-S),S,17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-P), DOC, P and T in spent media. 20 beta-S and S secretion increased and 17 alpha,20 beta-P decreased progressively with stage of maturation, but DOC was similar in all stages. P secretion was maximal and T lowest in M-stage spermatocysts, but when DOC (0.1 microM) was added to PrM or PoM spermatocysts, T output decreased. Taken together, the data suggest that 21-hydroxylating pathways, via direct and indirect mechanisms, affect accumulation of bioactive steroids (P and T) differentially by stage of spermatogenic development. Whether 21-hydroxylated progestins produced in shark testis have paracrine or endocrine actions in their own right remains to be investigated.

The profiles of testosterone (T) 11-ketotestosterone (11-KT), 17 alpha-hydroxy-4-pregnen-3-one (17-P), and 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-P) were determined in groups of spermiating male common carp (Cyprinus carpio) which were or were not mated with females and subjected to an increase in water temperature, a treatment which usually induces females to spawn. The steroid levels were correlated with changes in gonadotropin (GtH). All males mated with ovulatory females showed a GtH surge and spawned. Two distinct classes of these spawned males were differentiated based on their initial androgen levels and hormone profiles. Androgen levels were initially elevated in the "high" males. In these fish there was a very rapid shift in the steroidogenic pathway from androgen to progestogen production coincident with the GtH surge. In the "low" males, 17-P levels rose significantly in response to the GtH surge, but there was no steroidogenic shift. In the males mated with nonovulatory females, the levels of 17-P, 17,20 beta-P, T, and 11-KT all increased coincident with a small rise in GtH; there was no steroidogenic shift. In the unmated males, the steroid profiles were similar to those in the nonspawned fish, except that T and 11-KT levels were significantly lower in comparison. In all groups, 17-P rose higher than 17,20 beta-P, and 11-KT was generally the predominant androgen. A model is proposed which explains the steroidogenic shift in the "high" males. This involves the inhibition of androgen biosynthesis by 17,20 beta-P or by a related progestogen.

There is a rapid shift in the steroidogenic pathway from androgen to progestogen production in spawning male common carp, Cyprinus carpio. Experiments were conducted to determine the mechanism regulating this shift using in vitro cultures of testicular fragments and isolated sperm of spermiating male carp. The levels of 11-ketotestosterone (11-KT) continually increased for 48 h with or without gonadotropin (GtH) stimulation, suggesting that 11-KT is the principal androgen produced by carp testes. Ovine prolactin (oPRL) enhanced GtH-stimulated 11-KT production, but by itself had no effect. Gonadotropin, carp pituitary extract, and pregnenolone all enhanced the production of 11-KT, testosterone (T), and 17 alpha-hydroxyprogesterone (17-P) in a dose-dependent manner. No 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-P) was detected in response to any of these agents; 17 alpha,20 alpha-dihydroxy-4-pregnen-3-one (17,20 alpha-P) was not measured. Both 17,20 beta-P and 17,20 alpha-P inhibited 11-KT production in a dose-dependent manner in the presence of either GtH, 17-P, or T. Isolated sperm and testicular fragment preparations both produced 17,20 beta-P and approximately tenfold more 17,20 alpha-P when incubated with 17-P. Only testicular fragments, however, produced 11-KT. We conclude that androgen synthesis occurs only within somatic cells of common carp testes. GtH, and perhaps PRL, stimulates the production of steroid precursors that, under normal physiological conditions, are metabolized to androgens.(ABSTRACT TRUNCATED AT 250 WORDS)

We have shown a basic biophysical difference between clinically similar hand injuries and suggest that some rotary lawn mower injuries more closely resemble high-velocity missile injuries. A treatment protocol is suggested.

The effects of estradiol-17 beta (E2) and thyrotropin-releasing hormone (TRH) on prolactin (PRL) release were investigated using the organ-cultured rostral pars distalis (RPD) of the tilapia, Oreochromis mossambicus. Spontaneous PRL release into hyperosmotic medium increased in a dose-related manner following E2 pretreatment in vitro. In addition, TRH stimulated a dose-related increase in PRL release from E2-preincubated RPD's, but had no effect on tissues not previously exposed to E2. The maximal PRL response, nearly three times control levels, occurred at 50 nM TRH. Higher doses of TRH were less effective in stimulating PRL release. These findings indicate that TRH may be an important hypothalamic prolactin-releasing factor in the tilapia. Furthermore, the marked potentiation of the action of TRH on PRL release following exposure to E2 suggest that there may be a shift in the control of PRL secretion with changes in the reproductive state of the tilapia.

Occupational radiation exposure was measured using three film badges and one ring thermoluminescent dosimeter. The radiation dose in the hospital but outside the operating room was measured as zero for the 12-month period. The measured trunk dose in the operating room was 5 mrem, and the measured dose to the head and neck region was 227 mrem. For selected orthopedic procedures a ring thermoluminescent dosimeter was worn on the left ring finger (under a lead glove when appropriate) and measured 0 mrem. The measured occupational radiation exposure to the author was well below the recommendations of the U.S. National Committee on Radiation Protection for maximal permissible dose. However, caution is advised since the long-term biologic effects of exposure to low doses of radiation are not well known. Since many factors influence the amount of radiation to individual surgeons, the data obtained are not necessarily representative.

Thirty-six shoulders with recurrent anterior dislocation or subluxation in thirty-four adolescent patients were treated with a modified Bristow procedure. The average length of follow-up was five years and ten months. Postoperatively, two patients had recurrent anterior subluxation on one occasion and none had recurrent anterior dislocation. The average loss of external rotation was 10 degrees. Despite the fact that young patients have a high rate of recurrence after anterior dislocation or subluxation of the shoulder, the modified Bristow procedure is an effective method of treating recurrent anterior instability of the shoulder in adolescents.