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Oral malignant melanoma, which frequently invades the hard palate or maxillary bone, is extremely rare and has a poor prognosis. Bone morphogenetic protein (BMP) is abundantly expressed in bone matrix and is highly expressed in malignant melanoma, inducing an aggressive phenotype. We examined the role of BMP signaling in the acquisition of an aggressive phenotype in melanoma cells in vitro and in vivo. In five cases, immunohistochemistry indicated the phosphorylation of Smad1/5 (p-Smad1/5) in the nuclei of melanoma cells. In the B16 mouse and A2058 human melanoma cell lines, BMP2, BMP4, or BMP7 induces morphological changes accompanied by the downregulation of E-cadherin, and the upregulation of N-cadherin and Snail, markers of epithelial-mesenchymal transition (EMT). BMP2 also stimulates cell invasion by increasing matrix metalloproteinase activity in B16 cells. These effects were canceled by the addition of LDN193189, a specific inhibitor of Smad1/5 signaling. In vivo, the injection of B16 cells expressing constitutively activated ALK3 enhanced zygoma destruction in comparison to empty B16 cells by increasing osteoclast numbers. These results suggest that the activation of BMP signaling induces EMT, thus driving the acquisition of an aggressive phenotype in malignant melanoma.

Bone invasion is a critical factor in determining the prognosis of oral squamous cell carcinoma (OSCC) patients. Transforming growth factor β (TGF-β) is abundantly expressed in the bone matrix and is involved in the acquisition of aggressiveness by tumors. TGF-β is also important to cytoskeletal changes during tumor progression. In this study, we examined the relationship between TGF-β signaling and cytoskeletal changes during bone invasion by OSCC. Immunohistochemical staining of OSCC samples from five patients showed the expression of p130Cas (Crk-associated substrate) in the cytoplasm and phosphorylated Smad3 expression in the nucleus in OSCC cells. TGF-β1 induced the phosphorylation of Smad3 and p130Cas, as well as epithelial–mesenchymal transition (EMT) accompanied by the downregulation of the expression of E-cadherin, a marker of epithelial cells, and the upregulation of the expression of N-cadherin, or Snail, a marker of mesenchymal cells, in human HSC-2 cells and mouse squamous cell carcinome VII (SCCVII) cells. SB431542, a specific inhibitor of Smad2/3 signaling, abrogated the TGF-β1-induced phosphorylation of p130Cas and morphological changes. Silencing p130Cas using an short hairpin RNA (shRNA) or small interfering RNA in SCCVII cells suppressed TGF-β1-induced cell migration, invasion, EMT and matrix metalloproteinase-9 (MMP-9) production. Compared with control SCCVII cells, SCCVII cells with silenced p130Cas strongly suppressed zygomatic and mandibular destruction in vivo by reducing the number of osteoclasts, cell proliferation and MMP-9 production. Taken together, these results showed that the expression of TGF-β/p130Cas might be a new target for the treatment of OSCC bone invasion.

Invited for this month's cover picture is the group of Dr. Satoko Hayashi at Faculty of Systems Engineering and Chemistry at Wakayama University. The cover picture shows the linear Se(16) σ(16c–30e) interactions, illustrated by the molecular graph type on the optimized structure of the dicationic octamer of 1,5‐(diselena)cane. HOMO‐1 of ψ(462) is drawn on the structure, which is located predominantly on the Se atoms. The optimized structure is stable, due to the nice engagement between the (CH(2))(3) moieties. The contour maps of ρ(r) are also drawn on the molecular C (s) planes of the dicationic dimer and trimer to demonstrate clearly the existence of the interactions between Se atoms. Read the full text of their Full Paper at 10.1002/open.202100017.

We previously demonstrated that the immunostimulatory activity of CpG DNA is increased by the formation of polypod-like structures. The present study was designed to elucidate the mechanism underlying this increase. Tripodna (three pods) and hexapodna (six pods) were prepared. The cellular uptake of Alexa Fluor 488-labeled DNA samples was examined in several cell lines by measuring the MFI of cells. TNF-α release from RAW264.7 cells was measured after addition of polypodna containing CpG motifs. Dissociation of double stranded DNA was evaluated using FRET. Tripodna and hexapodna were efficiently taken up by macrophage-like RAW264.7 cells and dendritic DC2.4 cells, but not by fibroblast or endothelial cell lines. The uptake by RAW264.7 cells was highest for hexapodna, followed by tripodna, dsDNA, and ssDNA. The release of TNF-α from RAW264.7 cells was also highest for hexapodna. The ratio of TNF-α release to cellular uptake was highest for ssDNA, and lowest for dsDNA. Tripodna and hexapodna were more easily dissociated into single strands after cellular uptake than was dsDNA. The efficient cellular uptake and prompt dissociation into single strands can be directly related to the high immunostimulatory activity of polypod-like structured DNAs containing CpG motifs.

We have been investigating the potential use of cell-penetrating peptide-linked polymers as a novel penetration enhancer. Since previous in vivo studies demonstrated that poly(N-vinylacetamide-co-acrylic acid) bearing D-octaarginine, a typical cell-penetrating peptide, enhanced membrane permeation of biomolecules, its potential as an in vitro transfection tool was evaluated in this study. A plasmid DNA encoding green fluorescent protein (pGFP-C1), β-galactosidase, and bovine serum albumin (BSA) were used as model biomolecules. Anionic pGFP-C1 interacted electrostatically with cationic d-octaarginine-linked polymers. When the ratio of mass concentration of polymers to that of pGFP-C1 reached 2.5, complexes whose size and zeta potential were approximately 200 nm and 15 mV, respectively, were obtained. GFP expression was observed in cells incubated with complexes prepared under conditions in which the polymer/pDNA concentration ratio exceeded 2.5. The expression level elevated with an increase in the concentration ratio, but physicochemical properties of the complexes remained unchanged. Results suggested that free polymers contributed to pGFP-C1 internalization. Another cell study demonstrated that β-galactosidase premixed with polymers was taken up into cells in its active tetrameric form. Similar electrostatic interaction-driven complex formation was observed for BSA charged negatively in neutral solution. However, it appeared that the internalization processes of BSA differed from those of pGFP-C1. A mass concentration-dependent increase in internalized BSA was observed, irrespective of the polymer/protein concentration ratio. Due to frail interactions, polymers that were released from the complexes and subsequently immobilized on cell membranes might also contribute to membrane permeation of BSA.

The dynamic and static nature of extended hypervalent interactions of the BE···AE···AE···BE type are elucidated for four center–seven electron interactions (4c–7e) in the radical cationic dimers (1·+) and 4c–6e in the dicationic dimers (12+) of 1,5-(dichalcogena)canes (2: AE(CH2CH2CH2)2BE: AE, BE = S, Se, Te, and O). The quantum theory of atoms-in-molecules dual functional analysis (QTAIM-DFA) is applied for the analysis. Total electron energy densities Hb(rc) are plotted versus Hb(rc) – Vb(rc)/2 [= (ℏ2/8m)∇2ρb(rc)] at bond critical points (BCPs) of the interactions, where Vb(rc) values show potential energy densities at BCPs. Data from the fully optimized structures correspond to the static nature of the interactions. Those from the perturbed structures around the fully optimized ones are also plotted, in addition to those of the fully optimized ones, which represent the dynamic nature of interactions. The BE···AE–AE···BE interactions in 12+ are stronger than the corresponding ones in 1·+, respectively. ...

Keratin 17 (KRT17) has been suggested as a potential diagnostic marker of squamous cell carcinoma including oral squamous cell carcinoma (OSCC). The current study was conducted to clarify the function of KRT17 and its expression mechanism in OSCC. Immunohistochemical analyses were carried out to examine the expression of KRT17, GLI family zinc finger (GLI)-1, GLI-2, or cleaved caspase-3 in OSCCs. The expression of KRT17, GLI-1, or GLI-2 was investigated among OSCC cell lines, and the effects of loss-of-function of KRT17 or GLI, using siRNA or inhibitor, on the cell growth of the OSCC cell line HSC-2 particularly with respect to apoptosis were examined. Immunohistochemical analyses of tissue specimens obtained from 78 OSCC patients revealed that KRT17 was not observed in non-tumor regions but was strongly expressed at high frequencies in tumor regions. Knockdown of KRT17 increased the number of cleaved caspase-3-positive cells, leading to the reduction of cell number. Loss-of-function of GLI-1 or GLI-2 also increased the cell numbers of apoptotic cells positive for staining of Annexin-V and propidium iodide (PI) and the terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling (TUNEL) method, and induced DNA fragmentation. This inhibitory effect on cell growth was partially rescued by exogenous KRT17 expression. In the KRT17-positive regions in OSCCs, GLI-1 or GLI-2 was frequently detected, and the number of cells with cleaved caspase-3 positive was decreased. KRT17 promotes tumor cell growth, at least partially, through its anti-apoptotic effect as a result of the KRT17 overexpression by GLIs in OSCC.

We deposited a 4-inch crack-free aluminum nitride (AlN) layer on a flat sapphire substrate and a patterned sapphire substrate grown using metal-organic vapor phase epitaxy method. To use the 4-inch sapphire substrate, we introduce air voids in the AlN layer in the initial growth region. Moreover, we discovered that optical absorption exists in the AlN layer with air voids. The secondary ion mass spectrometry (SIMS) results show that the impurity concentrations are high at the regions where the air voids exist, though the growth conditions are same throughout the AlN layer. We considered that it is most probable that the optical absorption is mainly attributed to the complexes of Al and O. The origin of the optical absorption was identified as a deep emission band due to impurities such as carbon and oxygen around the air voids. In this study, it was possible to obtain a transparent AlN template without air voids by changing the growth conditions and the layer structure. In addition, we could further suppress the underlying layer with the air voids.

Interleukin (IL)-22 is a member of the IL-10 family. Its main targets are epithelial cells, not immune cells. We examined IL-22 signal transduction in oral squamous cell carcinoma (OSCC) cells. Immunohistochemical staining revealed that IL-22R was expressed more highly in OSCC compared to normal regions. An IL-22R signal was also observed in metastatic OSCC cells in the lymph node. RT-PCR showed that the human OSCC cell lines MISK81-5, HSC-3, HSC-4, SAS and SQUU-B expressed IL-22 receptor chains. Immunoblotting showed that IL-22 induced a transient tyrosine phosphorylation of STAT3 (pY705-STAT3) in MISK81-5 cells. The change in the serine phosphorylation of STAT3 was subtle during the examination periods. Simultaneously, pY705-STAT3 activation in HSC-3 cells was undetectable after IL-22 stimulation. Immunocytochemistry demonstrated that IL-22 induced the translocation of phosphorylated STAT3 into the nucleus of MISK81-5 cells. IL-22 temporarily upregulated the expression of anti-apoptotic and mitogenic genes such as Bcl-x, survivin and c-Myc, as well as SOCS3. IL-22 transiently activated ERK1/2 and induced a delayed phosphorylation of p38 MAP kinase, but negligibly involved the activation of NF-κB in MISK81-5 cells. MISK81-5 and SQUU-B cells treated with IL-22 showed mild cellular proliferation. MISK81-5, HSC-4 and SAS cells treated with IL-22 downregulated the keratinocyte differentiation-related genes compared with unstimulated cells. Conversely, STAT3 suppression by STAT3 siRNA strongly disrupted the downregulation of these genes by IL-22, but it did not significantly affect the activation of ERK1/2 by IL-22. The OSCC cells used in this study upregulated the expression of SERPINB3/4 (SCCA1/2), well-known SCC markers, following treatment with IL-22. These results indicate that IL-22 differentially activates the STAT3 signaling system depending on the type of OSCC. IL-22 may therefore play a role in tumor growth, cell differentiation and progression through STAT3-dependent and -independent pathways.

The crystalline quality of GaN and Al0.08Ga0.92N epitaxial layers on (100) β-Ga2O3 substrates was significantly improved by the facet-controlled growth method. The facets were controlled by changing the nitrogen ambient thermal annealing temperature. We demonstrated the high-crystalline-quality GaN and Al0.08Ga0.92N on β-Ga2O3 substrates, which were comparable to GaN and AlGaN on sapphire substrates using low-temperature buffer layers. This method is useful for the fabrication of vertical-type ultraviolet (UV) light-emitting diodes (LEDs) on β-Ga2O3 substrates. (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

We demonstrated activation annealing of Mg-doped p-type Al 0.17 Ga 0.83 N in different gases. The hole concentration of Al 0.17 Ga 0.83 N annealed in oxygen is higher than that annealed in nitrogen or air. A hole concentration of 1.3 × 10 16 cm -3 at room temperature was achieved by annealing in oxygen flow at 900 °C. Secondary ion mass spectroscopy shows that hydrogen dissociation from Mg-doped Al 0.17 Ga 0.83 N is found to be enhanced by annealing in a flow of oxygen, compared with annealing in a flow of nitrogen. We confirmed the effect of activation annealing in oxygen flow on the performance of UV light-emitting diode (LED). At a DC current of 100 mA, the output power of the LED annealed in oxygen flow at 900 °C is four times higher than that of the LED annealed in nitrogen flow at 800 °C.

Simon extracts are vitamin K(1)-rich food materials extracted from the leaves of the Simon sweet potato. Although vitamin K is known to stimulate bone formation, we postulated that Simon extracts also contain unknown biological compounds having the ability to regulate bone resorption. Here we prepared the vitamin K-free fraction from the Simon extracts and investigated the ability of this fraction on the differentiation of osteoclasts. A remarkable inhibitory effect of osteoclastogenesis was observed when osteoclast precursors were treated with this fraction in rat bone marrow culture systems as well as in a pure differentiation system using murine osteoclast precursor cell line. The vitamin K-free Simon extracts markedly suppressed severe bone destruction mediated by abundant osteoclasts associated with adjuvant-induced arthritis in rats. High performance liquid chromatography (HPLC) analysis revealed that the vitamin K-free Simon extracts contained three types of low molecular weight inhibitors for osteoclastogenesis; caffeic acid, chlorogenic acids and isochlorogenic acids. Among these substances, caffeic acid showed the most powerful inhibitory effects on osteoclastogenesis. Caffeic acid significantly suppressed expression of NFATc1, a key transcription factor for the induction of osteoclastogenesis. Our current study enlightened a high utility of the Simon extracts and their chemical components as effective regulators for bone resorption accompanied with inflammation and metabolic bone diseases.

V-ATPase is involved in the acidification of the microenvironment around/in solid tumors, such as oral squamous cell carcinoma (OSCC). V-ATPase is thought to induce tumor invasion and multi-drug resistance in several malignant tumors, and it also contributes to maintaining the intracellular pH under an acidic microenvironment by inducing proton extrusion into the extracellular medium. However, there is little information regarding the effects of V-ATPase inhibitors on OSCCs. In this study, the effects of a V-ATPase inhibitor, concanamycin A1 (CMA), on the proliferation and apoptosis of OSCC were investigated in vitro. We used four OSCC cell lines, MISK81-5, SAS, HSC-4 and SQUU-B. Acridine orange staining revealed that the red fluorescence was reduced in all of the low concentration CMA-treated OSCC cells, indicating that the acidification of vesicular organelles in the OSCCs was prevented by the treatment with low-concentration of CMA. CMA treatment induced apoptosis in MISK81-5, SAS and HSC-4 cells, but not in SQUU-B cells. The p-p38 expression was not altered in CMA-treated SQUU-B cells, but their levels were increased in the other cells. The Bax/Bcl-2 ratio in CMA-treated SQUU-B cells was dramatically decreased in comparison with that in the other cell lines treated with CMA. However, when the SQUU-B cells were treated with CMA and a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), the SQUU-B cells became more susceptible to the CMA-induced apoptosis. SAHA treatment led to a significantly decrease in the Bcl-2 expression in CMA-treated SQUU-B cells, resulting in a dramatically increased Bax/Bcl-2 ratio in comparison with that observed in the SQUU-B cells treated with CMA alone. These findings suggest that CMA could have an anti-tumor effect on OSCCs. In addition, combination of CMA with other agents, such as SAHA, could help improve the pro-apoptotic effects of CMA even in CMA-resistant OSCC cells.

Background: Recently, collagenous interodontoblastic fibers (IOF) were reported in some particular developmental stages and/or locations of the tooth. However, it remained unclear whether these fibers were identical to so-called von Korff fibers. Methods: To clarify this issue, we examined the developing mouse molar by three-dimensional reconstruction of 8 confocal images within a 6 μm-thick section using laser scanning confocal microscopy, and confirmed our findings using immunoelectron microscopy. Results: In the root pulp during circumpulpal dentin formation, the IOF stained weakly for type I collagen, but stained strongly for type III collagen by a double-staining technique. It could be clearly seen that many immunoreactive fibers ran spirally among the odontoblasts and entered the predentin. This distribution pattern of IOF was similar to that of the classical von Korff fibers. Furthermore, the existence of anti-type III reactive collagen fibrils between odontoblasts was confirmed, whereas IOF were not observed in the coronal pulp during circumpulpal dentin formation. Conclusions: This study presents for the first time, immunohistochemical observations which demonstrate the presence of IOF at least during root circumpulpal dentin formation and which reveal that type III collagen is a major component of IOF. © 1994 Wiley-Liss, Inc.

The enamel-free cusps of 1–4-day-old rat mandibular first molars were investigated using the monoclonal antibody En3 against rat amelogenin at light and electron microscopic levels in order to clarify whether the enamel-free cusp is virtually devoid of enamel. At 1 day after birth, there were presecretory ameloblast-like cells (PALCs), which were short and were not polarized, at the cusp tips. They were close to the outer enamel epithelium. Hematoxylin positive enamel matrix was not distinctly observed in the enamel-free cusp by light microscopy, but almost continuous immunofluorescence for amelogenin was detected at the interface between PALCs and dentin. The penetration of immunopositive material toward the dental pulp was also observed in the enamel-free cusp. At 4 day after birth, both in the frontal section and in the horizontal section, almost continuous immunofluorescence was recognized at the interface between PALCs and dentin in the enamel-free cusp. The penetration of amelogenin toward the dental pulp was not seen in the enamel-free cusp. By immunoelectron microscopy, immunolabelling was recognized in the Golgi apparatus of PALCs, in a layer of amorphous material at the interface between PALCs and dentin, and in stippled material-like substance in the intercellular space between PALCs. Although no basement membrane was observed beneath PALCs, they did not have Tomes' processes. These investigations suggest that PALCs in the enamel-free cusp differentiate into the secretory cells and that they can synthesize and secrete the amorphous material containing amelogenin at the interface between PALCs and dentin. The penetration of amelogenin toward the dental pulp might play a role in the interaction between PALCs and odontoblasts in the enamel-free cusp and/or the initiation of mineralization of predentin. © 1992 Wiley-Liss, Inc.

In order to examine the synthesis and secretion of enamel protein by ameloblasts in their early stages of development, immunohistochemical localization was carried out at light and electron microscopic levels using a monoclonal antibody produced in a preliminary experiment. Materials used were tooth germs of mandibular first molars of rats at 0-5 days after birth. Immunoblot analysis after two-dimensional electrophoresis revealed that antigen molecules recognized by the monoclonal antibody were amelogenins of 26-28 kDa (pI, 6.6-7.0). An immunohistochemical examination using this monoclonal antibody demonstrated that the presecretory ameloblasts in their early stages of differentiation both synthesized amelogenin and secreted through a classical merocrine secretory pathway. In some presecretory ameloblasts as well as ameloblasts we observed the distended cisternae of rough endoplasmic reticulum (rER) which demonstrated heterogenous immunolabelling. The immunolabellings were also detected in the predentin as well as the intercellular spaces of odontoblasts and dental pulp cells which indicated penetration of amelogenin from the presecretory ameloblast layer to the dental pulp. The presence of coated pits at the plasma membrane of odontoblasts in close proximity to enamel protein along with the immunolabelling of lysosomes of the odontoblasts suggests the phagocytosis of the enamel protein into the odontoblasts. These observations suggest the possibility that the penetration of enamel protein toward the dental pulp and odontoblasts plays a role in the interaction between ameloblasts and odontoblasts.

We studied the effects of platelet-derived growth factor-B (PDGF-B) and bone morphogenetic protein-2 (BMP-2) during the healing of mandibular closed fractures in rats by immunohistochemical methods. Unilateral closed fractures were created in the mandibles of thirty 12-week-old rats. BMP-2 was expressed during all stages of healing, but PDGF-B was expressed mainly in the early and middle stages, and not in the later stage of the healing process. We conclude that PDGF-B was associated with the proliferation and migration of primitive mesenchymal cells. BMP-2 was related to the differentiation of mesenchymal cells into osteoblasts and chondroblasts. PDGF-B and BMP-2 both have distinct regulatory effects on the healing of fractures.

The detailed distribution of types 1 and III collagen and fibronectin was studied in the developing mouse palatal shelf using a double immunofluorescence technique. Just prior to palatal shelf elevation, type I collagen showed denser localization on the nasal side than on the oral side of the middle hard palate region. Such a distribution extended as far as the posterior hard palate region but not to the soft palate region. In type III collagen and fibronectin, this uneven distribution was not so distinct even in the middle hard palate region during the same period. The correspondence of the most conspicuous region of this distribution of extracellular matrix components with the region of first shelf elevation suggests that the extracellular matrix, especially type I collagen, participates in palate development.

The distribution of types I and III collagen in mouse oral mucosa and the age-related changes over 3 days to 2 years of age were examined by immuno-fluorescence and -electron microscopy, with use of affinity-purified polyclonal antibodies. Immunofluorescence microscopy revealed that types I and III collagen existed in all tissues and at all ages examined. The staining intensity for type I collagen was stronger and increased more markedly in the lamina propria of the hard palate (HPlp) and gingiva (G), compared with that in the submucosa of the hard palate (HPsm) and the buccal mucosa (BM). The staining intensity for type III collagen was strong and increased markedly with age in all connective tissues examined. Examination of immunogold-labeled tissues demonstrated that most of the collagen fibrils were labeled for both type I and type III collagen, which suggests that they were hybrid fibrils containing both types of collagen. The quantitative evaluation of the labeling densities of gold particles revealed that the labeling density of type III collagen in BM and HPsm was higher and increased more rapidly during growth than in HPIp and G, while the labeling density of type I collagen was higher in HPIp and G. The fibril diameters in HPIp were larger and increased more rapidly during growth than in BM and HPsm. These studies are the first to demonstrate the distribution of types I and III collagen and their age-related changes in mouse oral mucosa. The results support previous suggestions that type I collagen may contribute to the stability of the connective tissue organization and that type III collagen may play an important role in the flexibility of the connective tissue of oral mucosa as well as in the regulation of the collagen fibril diameters in the tissue.

Annealing in oxygen ambient was found to be effective for realizing a high hole concentration in p-type Al0.17Ga0.83N:Mg. The maximum hole concentration obtained was 1.3×1016 cm-3 at room temperature. Hydrogen dissociation from Mg-doped Al0.17Ga0.83N is found to be enhanced by annealing in a flow of O2 compared with annealing in a flow of N2.

Retinoic acid (RA), one of the inducers of cleft palate in vivo , specifically increased the 125 I-epidermal growth factor (EGF) binding capacity of embryonic palatal mesenchymal cells; the increase was completely inhibited by actinomycin D, suggesting that transcription is required for this change. When the increase in EGF receptors was related to the stimulation of DNA synthesis by EGF in the presence of various concentrations of RA, the maximum stimulation of [ 3 H]-thymidine by EGF was at 10 −9 M RA, but the maximum increase in the number of EGF receptors was at 10 −6 M RA. Thus the increase in the number of EGF receptors cannot be related to EGF-stimulated DNA synthesis.

Both phenytoin (PHT) and glucocorticoid (GC) have been reported to be an effective teratogen for the production of cleft palate. The authors suggest the possibility that a part of GC-receptor to which PHT competitively bind (common receptor with PHT), participate in the production of cleft palate. In the present study, as one of the studies for the elucidation of the mechanism of cleft palate induction with PHT, we investigated the PHT-receptors and its relation with GC in the lung tissue of mice, which were either sensitive (CF1) or resistant (C57BL/6) to PHT or GC. Scatchard analysis of the specific binding of 14C-PHT to the cytosol protein revealed that the total capacity of PHT-receptor for CF1 (1,571 fmole/mg protein) was much greater than that for C57BL/6 (994 fmole/mg). The value of the Kd's for these strains, however, were 18.1 and 16.5 nM, respectively, indicating the absence of any great difference between both strains. The capacity of the common receptors with GC for CF1 (236 fmole/mg) was greater than that for C57BL/6 (126 fmole/mg). But, the value of the Kd's for these strains were 5.4 and 3.1 nM, respectively, indicating the absence of a great difference between the strains. The analysis indicated that the lung tissue cytosols of both strains also contain the proper receptor for PHT, which is in a much greater amount than that of the common receptor.(ABSTRACT TRUNCATED AT 250 WORDS)