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A band-to-band Coulomb interaction model for the refractive index spectra is presented of AlxGa1-xAs for 0

An accurate absorption model including Coulomb interaction and Urbach-broadened band edge has been demonstrated for direct bandgap semiconductors. We propose a steep-edged compound Lorentzian line-shape function for modeling the Urbach tail and the line broadening of exciton absorptions. The results of applying this fitting procedure to room-temperature and low-temperature absorption spectra of GaAs, InP, and InAs are presented, and a consistent set of band parameters are extracted. The analytical absorption model is suitable for a complete closed-form Kramers-Kronig transform of the absorption spectrum to obtain the refractive-index spectrum. [ABSTRACT FROM AUTHOR]

Solitary metastatic pituitary stalk tumors account for approximately less than 1% of all pituitary gland tumors and present difficulties in clinical diagnosis because most of them are clinically silent and usually too small to cause radiological changes. With the advance of microsurgical techniques, keyhole surgery is indicated to obtain a specimen for pathological diagnosis and possible removal of the tumor. Here, we reported a patient who has a history of advanced breast cancer and who complained of polyuria and polydypsia. Magnetic resonance images revealed a solitary tumor over the pituitary stalk. A right supraorbital craniotomy was performed and the pathological report confirmed the diagnosis of metastatic breast cancer. This is the first case report using keyhole surgery to confirm the pathology and improve the clinical symptoms. The relevant literature is also reviewed.

A method for total esophageal reconstruction when intestinal options are no longer available is presented. The technique described utilizes the parascapular microsurgical free flap, which is tubed and interposed between the cervical esophagus and the gastric remnant in the abdomen. The technique involves a well-recognized microsurgical flap and may be added to the armamentarium for total esophageal reconstruction.

In human breast carcinomas, overexpression of the macrophage colony-stimulating factor (CSF-1) and its receptor (CSF-1R) correlates with poor prognosis. To establish if there is a causal relationship between CSF-1 and breast cancer progression, we crossed a transgenic mouse susceptible to mammary cancer with mice containing a recessive null mutation in the CSF-1 gene (Csf1(op)) and followed tumor progression in wild-type and null mutant mice. The absence of CSF-1 affects neither the incidence nor the growth of the primary tumors but delayed their development to invasive, metastatic carcinomas. Transgenic expression of CSF-1 in the mammary epithelium of both Csf1(op)/Csf1(op) and wild-type tumor-prone mice led to an acceleration to the late stages of carcinoma and to a significant increase in pulmonary metastasis. This was associated with an enhanced infiltration of macrophages into the primary tumor. These studies demonstrate that the growth of mammary tumors and the development to malignancy are separate processes and that CSF-1 selectively promotes the latter process. CSF-1 may promote metastatic potential by regulating the infiltration and function of tumor-associated macrophages as, at the tumor site, CSF-1R expression was restricted to macrophages. Our data suggest that agents directed at CSF-1/CSF-1R activity could have important therapeutic effects.

The growth and metastases of many solid tumors are dependent on the recruitment of new blood vessels. Tumor angiogenesis is most likely initiated by paracrine release of growth factors that bind to their corresponding endothelial cell surface receptors. To determine whether angiogenesis and growth factor receptor expression are consistent findings in malignant melanoma, primary human melanomas were examined for mRNA expression of receptors for fibroblast growth factors (FGFR-1, FGFR-2), vascular endothelial growth factor (VEGFR-1, VEGFR-2), and the receptors Tiel and Tie2. Charts were reviewed and archival formalin-fixed, paraffin-embedded primary tumors were obtained from patients with thin (<1 mm; n = 10), intermediate (1 to 4 mm; n = 10), or thick malignant melanoma (>4 mm; n = 8). Also examined was whether melanoma cell lines could induce endothelial growth factor receptor synthesis by metabolic labeling. It was found that tumor vascularity did not correlate with clinical stage, melanoma thickness, or clinical outcome. It was also found that melanoma cell lines were not capable of directly regulating endothelial cell synthesis of growth factor receptors. However, expression of Tiel and VEGFR-2 mRNA by the tumor vasculature in select stage IA-IIB patients, and FGFR-1 mRNA expression by the tumor cells in the same clinical stages was found. The expression of these growth factor receptors did not correlate with clinical outcome. These data suggest that angiogenesis is not a prominent characteristic of primary malignant melanoma lesions and that the endothelial cell expression of Tiel and VEGFR-2 in vivo is probably not directly induced by the tumor.

Methemoglobinemia is a rare complication in individuals exposed to nitrates or nitrites. Whereas methemoglobinemia is a recognized potential complication in burn patients treated with topical 0.5% silver nitrate solution, no report of methemoglobinemia in burn patients has been present in the literature for more than 15 years. We raise consciousness about this complication with a case report of a 12-month-old child with necrotizing fasciitis resulting from a cutaneous flank infection. The patient developed cyanosis 20 days after initiation of topical treatment with 0.5% silver nitrate solution. Intravenous injection of methylene blue can restore normal blood oxygenation.

Uterine stromal macrophages change dramatically in density and morphology through the estrous cycle and during early pregnancy, whereas those in the mesometrial triangle do not undergo these changes. The mononuclear phagocytic growth factor, colony-stimulating factor-1 (CSF-1), regulates both the density and morphology of uterine macrophage populations, as shown by the fact that uterine macrophages are depleted and more rounded in the absence of CSF-1 caused by the osteopetrotic (csfm(op)) null mutation, compared to those of normal mice. Restoration of circulating CSF-1 to the nullizygous mice did not affect stromal macrophage density although it restored the population in the mesometrial triangle. This suggests CSF-1 regulation of these macrophage populations by local and humoral routes, respectively. Nevertheless, even in the absence of CSF-1, stromal macrophage population density varies 30-fold through the estrous cycle, suggesting the involvement in their regulation of factors other than CSF-1, such as the chemokines, which are chemoattractive for macrophages. The mRNA for the chemokines JE (MCP-1), C10, RANTES, and MIP1alpha are expressed in the uterus, with elevated levels observed on the first day of pregnancy. Such molecules, together with CSF-1, may play a role in modulating the complexities of uterine macrophage dynamics in response to sex steroid hormones and mating.

A1, a bcl-2 family member, has been identified as a hematopoietic-specific, early inducible gene. In this study it is shown that stable transfection of A1 into an interleukin-3 (IL-3)-dependent myeloid precursor cell line, 32D c13, leads to a retardation of IL-3 withdrawal-induced cell death similar to that observed with transfection of bcl-2. However, unlike bcl-2. A1 expression permits the accumulation of differentiated myeloid cells both before and after IL-3 withdrawal. Total cell accumulation, on the other hand, is considerably greater after IL-3 deprivation in the bcl-2 transfectant than in A1-expressing cells. Cells cotransfected with the two genes behave similarly to cells singly transfected with bcl-2, except that viability following IL-3 withdrawal is somewhat further enhanced. These results suggest that these two proteins have distinct roles that may be related to the divergent regulation of their expression during myeloid differentiation.

The human immunodeficiency virus (HIV) causes acquired immunodeficiency syndrome, which remains uniformly fatal in affected individuals. A common route of HIV transmission is via inoculation of contaminated blood, which may occur during surgical procedures. Surgeons may estimate their risk of HIV infection over a 30-year surgical career based on HIV prevalence among surgical patients, percutaneous injury rate per operation, and seroconversion rate. Surgeons can reduce their risk by various means, but the most pragmatic is by reducing the rate of percutaneous injury through optimal surgical technique and proper precautions.

The beta chemokines are a family of 8- to 12-kDa leukocyte chemoattractants that are typically produced by activated macrophages or lymphocytes. We examined the expression in primary macrophages of a recently described, and as yet functionally uncharacterized, murine beta chemokine, C10, and contrasted its regulation with that of several other beta chemokines. Although three other beta chemokines, macrophage inflammatory protein-1 alpha (MIP-1 alpha), JE, and RANTES, were all induced by LPS treatment of bone marrow-derived macrophages (BMM) and/or resident peritoneal macrophages (RPM), LPS stimulation of C10 was never observed. Conversely, IL-3 and granulocyte macrophage-CSF (GM-CSF) strongly induced C10 in both macrophage populations, whereas MIP-1 alpha and RANTES showed a weaker induction restricted to BMM. JE was strongly induced but only in BMM. Finally, IL-4 strongly induced C10 in a dose-dependent manner in both BMM and RPM but failed to stimulate any of the other three beta chemokines. The accumulation of C10 protein in culture supernatants paralleled the induction of mRNA, and the combination of IL-4 and GM-CSF led to enhanced protein levels. The expression of the C10 message in response to cytokines was completely blocked by cycloheximide, whereas the other three chemokines were all overexpressed in the presence of this inhibitor. These results demonstrate a sharp divergence between the regulation of C10 expression and that of other chemokines and suggest that this molecule may have distinct functions in host defense.

Fc gamma R plays an important role in host defense, triggering and/or facilitating many immunologic responses. Of the three defined Fc gamma Rs, Fc gamma RI (CD64) is not known to be constitutively expressed on normal PMN. We report here that there is markedly increased expression of Fc gamma RI on the PMN of normal, healthy blacks, detected by binding of monoclonal antibody to this receptor. This may have significant implications when multiracial data are pooled in studies of receptor expression as markers of response to various chemotherapeutic agents.

Acute ethanol exposure produces activation of the brain-pituitary-adrenal (BPA) axis, resulting in the release of ACTH, beta-endorphin, and glucocorticoids. While elevated levels of plasma glucocorticoids are also found after chronic ethanol administration, plasma ACTH and beta-endorphin are normal or reduced. It is also unclear whether chronic ethanol exposure results in tolerance to the stimulatory effect of ethanol on BPA activity. To determine the site and mechanism of ethanol action on the BPA axis we studied the CRF secretory profile in a superfused rat hypothalamic preparation after chronic ethanol administration in vivo and the CRF responses after acute ethanol exposure in vitro. Superfused hypothalami from normal and pair-fed control rats released CRF-like immunoreactive material (CRF-LI) in a pulsatile manner, with a mean (+/- SE) frequency of 5.1 +/- 0.7 pulses/h. In contrast, the pulse frequency of CRF-LI release from hypothalami of rats receiving chronic ethanol treatment (fed an alcohol-containing liquid diet for 2 weeks) increased dramatically; the basal mean CRF level, pulse amplitude, and pulse duration remained unchanged. Hypothalamic CRF content was decreased. This chronic ethanol exposure also altered the dose-response characteristics of CRF release when ethanol was introduced acutely, as a pulse, into the in vitro preparation. Acute exposure to 20 mg/100 ml ethanol produced greater release of CRF-LI from control hypothalami than from chronic ethanol-exposed hypothalami. A further elevation above basal levels was produced by 200 mg/100 ml ethanol in control, but not ethanol-exposed, hypothalami. Secretion of CRF from ethanol-exposed hypothalami in response to depolarizing concentrations of potassium chloride was suppressed. Chronic ethanol treatment had no effect on CRF-LI and CRF bioactivity responses to stimulation with acetylcholine. These findings suggest the presence of a high frequency pulse-generating mechanism for CRF release in the hypothalamus. This pulsatile secretory mechanism is altered by chronic ethanol exposure of the animals in vivo. Chronic intoxication resulted in tolerance to the stimulatory effect of ethanol on CRF release in vitro.