Whole-body cryotherapy enhances the expression of heat shock protein 70 and related hormones.

BACKGROUND: Whole-body cryotherapy (WBC) is used as a conditioning method for athletes. However, the scientific evidence for its effects is still insufficient. OBJECTIVE: To elucidate the effects of transient WBC on the expression of heat shock protein (HSP) 70 and the secretion of related hormones in humans. MATERIALS AND METHODS: The participants in this study were six healthy adult men. WBC was performed for 3 min in a booth at a temperature in the range of -150 to -120 degree C, and measurements were taken immediately before (Pre), immediately after (Post), and 60 min after WBC (Post60). For measurement of core body temperature (gastrointestinal temperature), participants ingested a capsule-type wireless temperature sensor. The body surface temperature was measured using a noncontact thermometer, and measurements were taken at four sites on the body surface (chest, abdomen, front of the thigh, and front of the lower thigh). Leukocyte count, lactate dehydrogenase, creatine kinase, hemoglobin, hematocrit, adrenaline, noradrenaline, cortisol, adrenocorticotropic hormone (ACTH), erythropoietin, and HSP70 in the collected blood were measured. RESULTS: The results showed a decrease in body surface temperature and an increase in noradrenaline and ACTH immediately after WBC. In addition, the core body temperature decreased 60 min after WBC, accompanied by an increase in HSP70 expression. CONCLUSION: WBC may increase HSP70 expression via noradrenaline and ACTH. The results of this study suggest the usefulness of WBC in triggering protein synthesis and the maintenance of immune function after training. doi.org/10.54680/fr22210110512.

Distribution of ASIC4 transcripts in the adult wild-type mouse brain.

Acid-sensing ion channel 4 (ASIC4) belongs to the ASIC gene family of neuronal proton-gated cation channels, and is the least understood subtype among the members. Previous studies of ASIC4 expression in the mammalian central nervous system have shown that ASIC4 is abundantly expressed in the spinal cord and in various brain regions, such as the cerebral cortex, the hippocampus, and the cerebellum. However, the detailed distribution of ASIC4 transcripts in mammalian brains still remains to be elucidated. In the present study, radioactive in situ hybridization histochemistry with an ASIC4-specific cRNA probe was performed on wild-type mouse brains, followed by X-gal staining experiments with Asic4-lacZ reporter mice Asic4tm1a(KOMP)Mbp. It was found that ASIC4 mRNAs were widely expressed throughout the wild-type brain, but preferentially concentrated in the olfactory bulb, the piriform cortex, the caudate putamen, the preoptic area, the paraventricular nucleus, the medial habenular nucleus, the pretectal area, the lateral geniculate nucleus, the amygdaloid complex, the superior colliculus, the interpeduncular nucleus, and the granule cell layer of the ventral hippocampus, and these results were in agreement with the X-gal-positive reactions observed in the mutant brain. In addition, X-gal staining combined with immunohistochemistry identified intense signals for ASIC4 transcriptional activity in most of the choline acetyltransferase (ChAT)-positive principal neurons located in the basal forebrain cholinergic nuclei. Our data provide useful information to speculate possible roles of ASIC4 in diverse brain functions.

Intraosseous tumors of the skull. A pictorial review.

Radiologists often encounter intraosseous tumors of the calvarium. Compared with parenchymal lesions, information is limited. In this review, we list the calvarial tumors and correlate the radiologic appearance with the pathologic findings. We discuss primary intraosseous tumors and tumor secondary to systemic disease as well as metastatic malignant tumor. Differentiation between primary tumors and tumors secondary to systemic disease can be difficult. Physicians should explore the systematic disease. In the case of primary tumors, it is important to verify any soft-tissue component since this is an important differential diagnostic feature with the potential for malignant transformation.

Identification of a novel fibroblast growth factor, FGF-22, preferentially expressed in the inner root sheath of the hair follicle.

We isolated cDNA encoding a novel fibroblast growth factor (FGF-22) (170 amino acids) from human placenta. Of the FGF family members, FGF-22, which appears to be a secreted protein, is most similar to FGF-10 and FGF-7 (approximately 46% and approximately 40% amino acid identities, respectively). The human FGF-22 gene was localized on chromosome 19p13.3. We also isolated mouse cDNA encoding FGF-22 (162 amino acids) from the skin. Mouse FGF-22 shows high homology (87% amino acid identity) to human FGF-22. Mouse FGF-22 mRNA was found to be preferentially expressed in the skin among the mouse adult tissues examined by Northern blotting analysis. By in situ hybridization, FGF-22 mRNA in the skin was found to be preferentially expressed in the inner root sheath of the hair follicle. Therefore, FGF-22 is expected to be a unique FGF that plays a role in hair development.

Absence of nuclear p16 from Epstein-Barr virus-associated undifferentiated nasopharyngeal carcinomas.

OBJECTIVE: Epstein-Barr virus (EBV) is detected in the majority of undifferentiated nasopharyngeal carcinomas (UNPCs, World Health Organization type III). However, the exact mechanism involved in the carcinogenesis of EBV-associated UNPCs remains to be elucidated. An important unresolved question is: how is the normal cell cycle deregulated during EBV-associated UNPC development? The p16CDKN2 gene encodes a nuclear protein, p16, which inhibits the D-type cyclin/cyclin-dependent kinase complexes that phosphorylate the retinoblastoma gene product (pRb), thus blocking G1 cell cycle progression. The objective of this study was to determine whether p16 absence is involved in the development of EBV-associated UNPCs. METHODS: We performed immunohistochemistry to detect p16 and pRb and in situ hybridization to detect EBV-encoded small RNA (EBER) in UNPCs from 28 patients. RESULTS: No p16 was detected in 23 of 28 UNPCs (82.1%), whereas pRb was expressed in all those examined and EBER was detected in 22 of 28 (78.6%). The absence of p16 was associated with the presence of EBER in UNPCs (P < .0001): none of the 22 EBER+ UNPCs expressed p16, whereas 5 of 6 EBER- UNPCs did. CONCLUSION: Our data suggest that loss of p16-related cell cycle regulation plays an important role in the development of EBV-associated UNPCs.

Antibiotic stress induces a large amount of outer membrane protein in Pseudomonas aeruginosa.

To investigate the bacterial response to antibiotic stress, we analyzed the outer membrane proteins of Pseudomonas aeruginosa grown in the presence of a sub-minimum inhibitory concentration of antibiotics. Among the antibiotics tested, fluoroquinolones and streptonigrin induced a large amount of outer membrane protein with a molecular mass of 43 kDa. This protein is most likely the stress-responsive protein, since the quinolone-resistant mutants with a higher minimum inhibitory concentration of antibiotic than the wild-type strain produced a large amount of 43-kDa protein only in the presence of sub-minimum inhibitory concentration of the mutants itself, but not that of the antibiotic-susceptible wild-type strain. The sequence of N-terminal 15 amino acids of the 43-kDa protein was identical to that of pyocin R1. However, purified pyocin R1 failed to accumulate in the outer membrane. Thus, we concluded that the 43-kDa protein (pyocin R1) is the antibiotic-stress-induced outer membrane protein.

Comparison of the expression of three highly related genes, Fgf8, Fgf17 and Fgf18, in the mouse embryo.

In mammals, 16 members of the Fgf family have so far been described with diverse roles in embryonic cell growth and differentiation. Here, we report the expression from early streak stage to midgestation of two newly-identified murine genes, Fgf17 and Fgf18, that are most closely related to Fgf8 (63.7% and 56.8% identical, respectively, at the amino acid level). Fgf17 is expressed during gastrulation but at lower levels than Fgf8, while Fgf18 RNA is not expressed until later, in paraxial mesoderm. In the developing tail bud, each Fgf gene shows a different pattern of transcription. Distinct and overlapping expression patterns are also described in the developing brain and limbs.

Structure and expression of the mRNA encoding a novel fibroblast growth factor, FGF-18.

We isolated the cDNA encoding a novel member (207 amino acids) of the fibroblast growth factor (FGF) family from rat embryos. Because this protein is the 18th documented member of the FGF family, we tentatively termed it FGF-18. We have also determined mouse and human FGF-18 with high amino acid identity (99.5 and 99.0%) to rat FGF-18, respectively. Among FGF family members, FGF-18 is most similar (52.7% amino acid identity) to FGF-8 and FGF-17. FGF-18 has a typical signal sequence at its amino terminus. Recombinant rat FGF-18, which was efficiently secreted by High Five insect cells infected with recombinant baculovirus containing the cDNA, induced neurite outgrowth in PC12 cells. The expression of FGF-18 mRNA was examined in adult rat tissues and embryos by Northern blotting analysis and in situ hybridization. FGF-18 mRNA of approximately 2. 7 kilobases was preferentially detected in the lung among adult rat tissues examined. In rat embryos, FGF-18 mRNA was detected in several discrete regions at embryonic days 14.5 and 19.5 but not at E10.5. The temporal and spatial patterns of FGF-18 mRNA expression in embryos are quite different from those of FGF-8 and FGF-17 mRNAs reported. The present results indicate that FGF-18 is a unique secreted signaling molecule in the adult lung and developing tissues.

Structure and expression of a novel fibroblast growth factor, FGF-17, preferentially expressed in the embryonic brain.

We isolated the cDNA encoding a novel member (216 amino acids) of the fibroblast growth factor (FGF) family from rat embryos. As this protein is the 17th documented member of the FGF family, we tentatively termed it FGF-17. We have also determined the structures of mouse and human FGF-17 with high amino acid identity (100 and 98.6%) to rat FGF-17, respectively. Among FGF family members, FGF-17 is most similar (53.7% amino acid identity) to FGF-8. FGF-17 has a typical signal sequence at its amino terminus. As expected, recombinant rat FGF-17 was efficiently secreted by High Five insect cells infected with recombinant baculovirus containing the cDNA indicating that FGF-17 is a secreted protein. FGF-17 mRNA of approximately 2.1 kb was detected in rat embryos at E14.5, but not at E10.5 and E19.5 by Northern analysis. The mRNA was found to be preferentially expressed in the neuroepithelia of the isthmus and septum of the rat embryonic brain at E14.5 by in situ hybridization. The present results indicate that FGF-17 might be a novel secreted signaling molecule in the induction and patterning of the embryonic brain.

Involvement of cell-mediated killing in apoptosis in histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease).

Histiocytic necrotizing lymphadenitis, also called Kikuchi-Fujimoto (KF) disease, is a benign disorder characterized histologically by paracortical necrotic foci surrounded by histiocytic aggregates. We analysed affected lymph node tissues from 34 patients with the disease in an attempt to elucidate its histogenesis. The 'necrotizing' cells showed typical apoptotic changes, including cell shrinkage and condensed and fragmented nuclei. Apoptotic bodies with a peculiar ultrastructure were demonstrated, and DNA fragmentation was detected in these cells by in situ end labelling. Immunostaining for the apoptosis-regulating proteins bcl-2, bax, c-myc and p53 failed to show their involvement in KF disease. However, perforin, a killer cell-specific cytolytic protein essential for provoking apoptosis in target cells, was found to be expressed abundantly by the infiltrating cells, which were thought to be cytotoxic T-lymphocytes. Perforin-expressing cells were present in the apoptotic foci of 28 of the 34 patients (82.4%). Virtually no cells containing perforin granules were present in non-pathological regions, lymph node tissues from control subjects with reactive or tuberculous lymphadenitis or those from patients with KF disease with negligible apoptosis. Therefore, the 'necrosis' associated with KF disease appears to be attributable to trans apoptotic death of the killer cell target in the affected nodes. We propose that KF disease should be called apoptotic lymphadenitis.