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1 Affected individuals presented with variable skeletal abnormalities and neurodevelopmental defects.
2    Panx3-knockout (KO) mice have more severe skeletal abnormalities than those of Cx43-KO mice.
3 r characterized by congenital heart disease, skeletal abnormalities, and failure to thrive.
4 by poikiloderma, small stature, sparse hair, skeletal abnormalities, increased risk of osteosarcoma,
5 indicated to minimize the age-induced muscle skeletal adaptations.
6 alities in neurologic function as well as in skeletal and cardiac muscle defects.
7          Desmin (DES) mutations cause severe skeletal and cardiac muscle disease with heterogeneous p
8 ical and fossil record, even when associated skeletal and DNA preservation is poor.
9 re described, with specific attention toward skeletal and electroactive tissues, such as cardiac, ner
10 cal disorders, cancer, organismal injury and skeletal and muscular disorders, as well as networks of
11  to the human phenotype of short stature and skeletal anomalies in a heterozygous Bmp2-knockout mouse
12 ost important reactions for the formation of skeletal C-C linkages.
13 relation was seen between the dental age and skeletal Class II.
14 ents for the treatment of metastasis and for skeletal complications in prostate cancer patients.
15                   These findings explain the skeletal contact frequently observed in human SS and may
16 C in cells expressing type I collagen led to skeletal defects and hypophosphatemia.
17 ncy results in failure in bone formation and skeletal deformation.
18 , along with the observed slight decrease in skeletal density, we conclude that there must be biochem
19 espite the very different functions of their skeletal derivatives in jaw support and sound transducti
20  of heparan sulfate (HS), important for both skeletal development and hematopoiesis, through the form
21 as KLF10, plays important roles in mediating skeletal development and homeostasis in mice.
22 t, muscle weakness, anomalies in cranial and skeletal development, and reduced aggressiveness.
23 y disordered phosphoprotein, in chick embryo skeletal development, and using circular dichroism and m
24 terize various biophysical properties of the skeletal DHPR beta subunit beta1a Removal of the intrins
25 is of key importance in the understanding of skeletal disease.
26    Spondylocarpotarsal synostosis (SCT) is a skeletal disorder characterized by progressive vertebral
27            Osteoporosis is a common systemic skeletal disorder resulting in bone fragility and increa
28 ortedly cause frontometaphyseal dysplasia, a skeletal disorder with unknown pathogenesis.
29  mTORC1 and autophagy in the pathogenesis of skeletal disorders and suggest potential therapeutic app
30 with joint hypermobility, contractures, mild skeletal dysplasia and high myopia.
31 ling abnormalities have been associated with skeletal dysplasia in humans, and our findings present o
32 severe microcephaly, craniofacial anomalies, skeletal dysplasia, and neonatal lethality.
33 decreases SOX9 expression and causes a human skeletal dysplasia, identifying a mechanism that regulat
34 old, whereas GAC repeats are associated with skeletal dysplasias and expand from the normal five to a
35 cus heterogeneity characterizes a variety of skeletal dysplasias often due to interacting or overlapp
36 haped cartilage structures (Meckel, ribs and skeletal elements in developing limbs), the transverse i
37 nt knowledge regarding the roles of Panx3 in skeletal formation and address the potential for new the
38                                           In skeletal formation, Panx3 and Cx43 are the most abundant
39                            An improvement in skeletal glucose uptake rate was also observed in obese-
40 evelopment and essential for bone formation, skeletal growth and postnatal homeostasis.
41 stic lineage and have important functions in skeletal homeostasis.
42                                              Skeletal injuries were coupled with cryoablation to crea
43 tic breast cancer patients, often leading to skeletal injuries.
44              Purpose To determine indexes of skeletal integrity by using computed tomographic (CT) tr
45                                           In skeletal lesions from patients with metastatic PCa, hist
46 models of advanced breast cancer in relevant skeletal locations.
47 d cartilage dysplasia, but the mechanisms of skeletal manifestations remain unknown.
48  and lean mass.Bone mineral density and lean skeletal mass are heritable traits.
49  with peak growth at 90% of final height and skeletal maturity closely reflecting growth remaining.
50 ight velocity to normalized heights and hand skeletal maturity radiographs.
51 rity standard with its close relationship to skeletal maturity represents a significant advance allow
52 re considered adults based on average age of skeletal maturity.
53                                              Skeletal metastases, the leading cause of death in advan
54 fect zooplankton development, physiology and skeletal mineralization status, potentially reducing the
55 steonecrosis of the jaw, kidney dysfunction, skeletal morbidity rate (mean number of skeletal-related
56 ry end points included time to first SRE and skeletal morbidity rate (SMR).
57 l hematologic cancer that causes significant skeletal morbidity.
58 ificant reductions in GU in multiple tissues-skeletal muscle (36.4%), liver (16.1%), brown adipose (2
59 iet and exercise weight-loss intervention on skeletal muscle (SM) mass and selected organs over 2 y u
60  protein phosphorylation that occur in mouse skeletal muscle 1 h after a bout of electrically evoked
61 me profiling of individual proteins in human skeletal muscle after a high-fat diet and resistance exe
62 s chemokine and cytokine expression in mouse skeletal muscle after exercise and facilitates molecular
63 esulted in significant lowering of blood and skeletal muscle ammonia, increase in lean body mass, imp
64 es insulin's metabolic actions in the liver, skeletal muscle and adipose tissue.
65 tes muscle pathology and improves diaphragm, skeletal muscle and cardiac function.
66 pression, restores SERCA function, mitigates skeletal muscle and cardiac pathology, improves muscle r
67 ntary and obese populations, but rarely with skeletal muscle and elite athlete phenotypes.
68 dine receptor ion channel RyR1 is present in skeletal muscle and has a large cytoplasmic N-terminal d
69 exercise, IL-6 is synthesized by contracting skeletal muscle and released into circulation.
70 rst time the presence of ACSL6 mRNA in human skeletal muscle and the role that ACSL6 plays in lipid s
71 lin resistance to increase glucose uptake in skeletal muscle and therefore represents an important al
72 duced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycemia counterregulati
73 ivity was higher, whereas sensitivity of the skeletal muscle and white adipose tissue was lower in HF
74                                              Skeletal muscle atrophy due to excessive protein degrada
75 ay protect against the inflammation-mediated skeletal muscle atrophy which occurs in sarcopenia and c
76 NAs, miRs) have been shown to play a role in skeletal muscle atrophy, but their role is not completel
77 ported to be elevated in several settings of skeletal muscle atrophy.
78  breakdown, and device failure of engineered skeletal muscle bio-bots as a result of degradation by t
79 ject of intense interest within the field of skeletal muscle biology.
80 a lower capacity for fatty acid oxidation in skeletal muscle biopsies, along with enhanced efficiency
81 stimulated glucose uptake in human and mouse skeletal muscle by blocking the translocation of GLUT4 t
82  is a key regulator of glucose metabolism in skeletal muscle by directly controlling the transcriptio
83 ein optic atrophy 1 (OPA1) in differentiated skeletal muscle by reducing OPA1 gene expression in an i
84 Y POINTS: Severe burns result in significant skeletal muscle cachexia that impedes recovery.
85    ABSTRACT: The maximum velocity at which a skeletal muscle can shorten (i.e. the velocity of slidin
86 ApN proves to be a powerful protector of the skeletal muscle capable of reversing the disease progres
87 small heat shock protein (HspB8) in ischemic skeletal muscle cells and enhanced ischemic muscle autop
88 odel of insulin-stimulated glucose uptake in skeletal muscle cells by implicating p41ARC as a new com
89 gs between identified spinal motoneurons and skeletal muscle cells in larval zebrafish.
90 t that SIRT6 depletion in cardiac as well as skeletal muscle cells promotes myostatin (Mstn) expressi
91    In vitro (macrophages, endothelial cells, skeletal muscle cells under normal and hypoxia serum sta
92 of stem cell myogenesis (transformation into skeletal muscle cells) includes several stages character
93 ARP2/3 subunit p41ARC is a PAK1 substrate in skeletal muscle cells.
94 panded AR causes damage to motor neurons and skeletal muscle cells.
95                                              Skeletal muscle combines multiple signals that contribut
96 ents of circadian enzyme activities in mouse skeletal muscle confirmed that such timing separation oc
97 secrete cytokines, including IL-6, to repair skeletal muscle damage.
98 er, characterization of the DNA methylome of skeletal muscle demonstrates numerous local methylation
99                                Regulation of skeletal muscle development and organization is a comple
100                                              Skeletal muscle development requires fusion of mononucle
101 Myoblast fusion is an indispensable step for skeletal muscle development, postnatal growth, and regen
102 h1 signaling pathway and miRNAs regulate the skeletal muscle development.
103 ellular syncytial formation is a hallmark of skeletal muscle differentiation.
104 , including reductions in cardiac output and skeletal muscle diffusion capacity.
105 is a common form of congenital nondystrophic skeletal muscle disease characterized by muscular weakne
106 EY POINTS: Fibrosis occurs secondary to many skeletal muscle diseases and injuries, and can alter mus
107  only help to unravel the molecular basis of skeletal muscle diseases, but also provide a roadmap for
108 yosin storage myopathy (MSM) is a congenital skeletal muscle disorder caused by missense mutations in
109 cise training in obese mice with cardiac and skeletal muscle disruption of the Autophagy related 7 ge
110 e that exhibits anti-inflammatory effects on skeletal muscle exposed to acute and chronic inflammatio
111               In adult mice fed normal chow, skeletal muscle expression of insulin receptor beta and
112                                              Skeletal muscle fiber atrophy develops in response to se
113                               Multinucleated skeletal muscle fibers form through the fusion of myobla
114              These findings demonstrate that skeletal muscle fibers release exosomes which can exert
115  is a synapse formed between motoneurons and skeletal muscle fibers that is covered by Schwann cells
116 enes implicated in structure and function of skeletal muscle fibres (ACTG1), neuronal maintenance and
117                                     However, skeletal muscle fibres were hypotrophic and their nuclei
118      Understanding the mechanisms that drive skeletal muscle formation will not only help to unravel
119 ce that miR-29a and miR-29c are increased in skeletal muscle from patients with type 2 diabetes and a
120 mitochondrial BCAA management is impaired in skeletal muscle from T2D patients.
121 nces, urge caution in applying CR to improve skeletal muscle function across the lifespan in humans.
122         Mitochondrial health is critical for skeletal muscle function and is improved by exercise tra
123            BPA and TBBPA both interfere with skeletal muscle function through divergent mechanisms th
124                        Our results establish skeletal muscle glycogen as the source of TCA cycle expa
125 s is tightly regulated to ensure appropriate skeletal muscle growth and repair.
126 ro myogenesis and in conditions that promote skeletal muscle growth in vivo.
127 ite cells (PSCs) are important for postnatal skeletal muscle growth, and Notch1 signaling pathway and
128                              Whereas damaged skeletal muscle has a profound capacity to regenerate, h
129 nship between neuromuscular transmission and skeletal muscle hyperexcitability.
130 letal muscle mass, was strongly increased in skeletal muscle in a mouse model of stroke.
131  and longer term (8.5 and 18.5 months) CR on skeletal muscle in male and female C57Bl/6 and DBA/2 mic
132                   Due to the central role of skeletal muscle in whole-body metabolism, we aimed at st
133 ing computed tomography scans, we calculated skeletal muscle index (muscle area at the third lumbar v
134  These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin r
135                 Here, using an acute sterile skeletal muscle injury model combined with irradiation,
136                        Lack of HO-1 augments skeletal muscle injury, evidenced by increased creatinin
137 Ps orchestrates the regenerative response to skeletal muscle injury.
138  potential pharmacological target to improve skeletal muscle insulin sensitivity.
139                                              Skeletal muscle is the major site for insulin-stimulated
140                                  HFD altered skeletal muscle lipid profiles and up-regulated genes in
141 mplement previous studies on ammonia-induced skeletal muscle loss and lay the foundation for prolonge
142                                Sarcopenia or skeletal muscle loss is a frequent, potentially reversib
143 an body mass, improved grip strength, higher skeletal muscle mass and diameter, and an increase in ty
144 ostatin inhibition would improve recovery of skeletal muscle mass and function after cerebral ischemi
145  current RDA or twice the RDA (2RDA) affects skeletal muscle mass and physical function in elderly me
146                 ABSTRACT: The maintenance of skeletal muscle mass is essential for health and quality
147  found that PGC1beta progressively decreases skeletal muscle mass predominantly associated with loss
148  generate a mechanically induced increase in skeletal muscle mass, but the mechanism(s) through which
149 of myostatin, a master negative regulator of skeletal muscle mass, was strongly increased in skeletal
150 stantly sensing and responding to changes in skeletal muscle metabolism induced by contractile activi
151  In this study, we measured the stiffness of skeletal muscle myofibrils in rigor.
152  missense mutations in the beta-cardiac/slow skeletal muscle myosin heavy chain rod.
153                                The increased skeletal muscle myostatin expression, reduced mammalian
154 act myofibers were laser microdissected from skeletal muscle of 18 sIBM patients and analyzed by a se
155 ) similar to what is observed in contracting skeletal muscle of humans, and may be an important contr
156 se gene expression and enzymatic activity in skeletal muscle of mice in the corticosterone group rela
157 transition in fully activated fibers of fast skeletal muscle of the rabbit occurs during transition f
158 itochondrial (Mt) biogenesis and function in skeletal muscle of young horses.
159                        Here, we investigated skeletal muscle pathology in myofibers and myofibrils is
160 a-lowering therapy results in improvement in skeletal muscle phenotype and function and molecular per
161             SIRT6-KO mice showed degenerated skeletal muscle phenotype with significant fibrosis, an
162 ing 241 exercise-responsive genes related to skeletal muscle plasticity.
163                    A clock gene expressed in skeletal muscle plays a bigger role in regulating sleep
164 ues, we hypothesized that OPG-Fc, a bone and skeletal muscle protector, acts synergistically with bet
165 mality in cirrhosis that results in impaired skeletal muscle protein synthesis and breakdown (proteos
166                     In the young population, skeletal muscle pump was found to drive blood pressure c
167            Additionally, burn injury induced skeletal muscle regeneration, satellite cell proliferati
168                                              Skeletal muscle regrowth following a burn injury require
169 lect nonsteroidal anti-inflammatory drugs or skeletal muscle relaxants (moderate-quality evidence).
170                                              Skeletal muscle relaxants are effective for short-term p
171 uscle-specific enzyme in more differentiated skeletal muscle remain unknown.
172 m in several tissues; however, their role in skeletal muscle remains poorly characterized.
173 ferative hematopoietic system, whereas TL in skeletal muscle represents a minimally replicative tissu
174 uman alpha-cardiac myosin S1 and rabbit fast skeletal muscle S1.
175 rformed clonal multicolor lineage tracing of skeletal muscle stem cells (MuSCs) to address these ques
176                 Activity of satellite cells, skeletal muscle stem cells, is altered following a burn
177 e results provide an approach for generating skeletal muscle that is potentially applicable to other
178 ry aim of this study was to determine in rat skeletal muscle the influence of a brief (two weeks) HFD
179 ectly engages nutrient signaling pathways in skeletal muscle to maintain systemic glucose homeostasis
180                        We conclude that fast skeletal muscle troponin sensitizers constitute a potent
181 iated with CCL induces an anabolic effect in skeletal muscle undergoing regrowth after a period of at
182 3 transcript and protein expression in mouse skeletal muscle using Kcne3(-/-) tissue as a negative co
183 ts suggest that multi-faceted alterations to skeletal muscle venular function in OZR may contribute t
184                             For the shift in skeletal muscle venular function with development of the
185  KO results in fatal cardiomyopathy, whereas skeletal muscle was asymptomatic.
186               EEF1A2-deficient zebrafish had skeletal muscle weakness, cardiac failure and small head
187 al interactions among various organs: liver, skeletal muscle, adipose tissue, brain, and the endocrin
188                                           In skeletal muscle, agrin binds with high affinity to lamin
189 rm this hypothesis by showing that, in human skeletal muscle, and in contrast to the current view, th
190 r in the liver, nervous system, heart, lung, skeletal muscle, and intestine and illustrate how macrop
191 e 6 (ACSL6) mRNA is present in human and rat skeletal muscle, and is modulated by nutritional status:
192 we have performed transcriptomic analysis in skeletal muscle, and plasma metabolomics from subjects w
193 s limited such that it is only detectable in skeletal muscle, heart, brain and spinal cord.
194                                           In skeletal muscle, however, its role during physiological
195 acutely alter the DNA methylation profile of skeletal muscle, indicating that DNA methylation constit
196         Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging.
197 gic receptors, which are mainly expressed in skeletal muscle, is significantly reduced in dystrophic
198 strate uptake and protein accretion rates in skeletal muscle, late gestation control (CON) (n = 8) an
199                                              Skeletal muscle, liver, and plasma samples were analyzed
200 ons in other metabolic tissues (e.g., liver, skeletal muscle, pancreas) through lipotoxicity and infl
201 ocking out or restoring BMAL1 exclusively in skeletal muscle, respectively.
202 energy and substrate metabolism in liver and skeletal muscle, resulting in hepatic ketogenesis and gl
203 ly expressed with high levels in cerebellum, skeletal muscle, thymus and kidney.
204  selectively over-expressing PGC1beta in the skeletal muscle, we have found that PGC1beta progressive
205               Using cultured cells and mouse skeletal muscle, we show that TDP-43 acetylation-mimics
206 body carnitine pool is primarily confined to skeletal muscle, where it regulates carbohydrate (CHO) a
207 ression of the cytokine unpaired 2 (Upd2) in skeletal muscle, which acts as a myokine to control gluc
208 TDP-43 pathology in cultured cells and mouse skeletal muscle, which can be cleared through an HSF1-de
209 ticular, damage to mitochondrial proteins in skeletal muscle, which is a loss of mitochondrial proteo
210 connective tissue growth factor by Pofut1 in skeletal muscle, with additional effects on alpha dystro
211 genic non-coding RNA with MyoD-regulated and skeletal muscle-restricted expression that promotes the
212 nism for increasing metabolic power in human skeletal muscle.
213 hence, it may affect regeneration of injured skeletal muscle.
214 n ensure increased oxygen delivery to active skeletal muscle.
215 ed the expression of myogenic markers in the skeletal muscle.
216 for glucose metabolism and insulin action in skeletal muscle.
217 o a strategy to combat fatty degeneration of skeletal muscle.
218 ue alterations in glucose homeostasis in the skeletal muscle.
219 For example, cnrip1b is expressed in forming skeletal muscle.
220  kidneys and on urea production by liver and skeletal muscle.
221 ype IA fibers, and mitochondrial function in skeletal muscle.
222 slocation of GLUT4 to the plasma membrane in skeletal muscle.
223  signaling and glycogen synthase activity in skeletal muscle.
224  diet (HFD) caused insulin resistance in rat skeletal muscle.
225 alities of other organ systems, particularly skeletal muscle.
226 id metabolism, and insulin responsiveness in skeletal muscle.
227 begun to explore the role of this protein in skeletal muscle.
228 luding the hypothalamus, adipose tissue, and skeletal muscle.
229 key receptor for the MSTN/activin pathway in skeletal muscle.
230 usal role in overload-induced hypertrophy of skeletal muscle.
231 ponses in highly metabolic tissues, such as, skeletal muscle.
232 bolic programming of glycolytic myofibers in skeletal muscle.
233 s (MICs) on protein phosphorylation in mouse skeletal muscle.
234 the age-related defects that occur in rodent skeletal muscle.
235 ion of the reconstructed microcirculation in skeletal muscle.
236  in lipid synthesis in both rodent and human skeletal muscle.
237 ween the liver, adipose tissue, pancreas and skeletal muscle.
238 d impact the transcriptome and metabolome of skeletal muscle.
239  along with its known aerobic effects in the skeletal muscle.
240 dance on a protein-by-protein basis in human skeletal muscle.
241 such as cardiac, nerve, bone, cartilage, and skeletal muscle.
242 pression of the DUX4 transcription factor in skeletal muscle.
243 in red wine, improves exercise endurance and skeletal-muscle oxidative metabolism in animals and may
244 nsforming growth factor-beta1 (TGF-beta1) in skeletal muscles and at their NMJs.
245 te is significantly reduced in the liver and skeletal muscles of Cry-deficient mice.
246 al hypertrophic growth were also observed in skeletal muscles of these mice.
247 thin hours of exposure to hypoxia in in vivo skeletal muscles remain unexplored.
248 d to a synaptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremitie
249                                              Skeletal muscles were functionally impaired from 2 month
250                         KEY POINTS: In human skeletal muscles, the current view is that the capacity
251 bility and contractility of both cardiac and skeletal muscles.
252  proteins that interact with PABPN1 in mouse skeletal muscles.
253 which affects the localization of hVps13A in skeletal muscles.
254 imal limb weakness and nuclear aggregates in skeletal muscles.
255 ck filament length is reduced in cardiac and skeletal muscles.
256 ts and potentiates their positive effects on skeletal muscles.
257 r neurons and subsequent atrophy of proximal skeletal muscles.
258                 Inadequate insulin action in skeletal myocytes contributes to hyperglycemia in diabet
259 nduce aging-related phenotypes in cis within skeletal myofibers and in trans within satellite cells a
260 r, premature postnatal deletion of Pofut1 in skeletal myofibers can induce aging-related phenotypes i
261                           Pofut1 deletion in skeletal myofibers reduced NotchR signaling in young adu
262 ut also provide a roadmap for recapitulating skeletal myogenesis in vitro from pluripotent stem cells
263 rome characterized by variable expression of skeletal, neurological, and immunological abnormalities.
264 utcomes, including bone loss that may weaken skeletal or periodontal strength.
265                For decades, the mechanism of skeletal patterning along a proximal-distal axis has bee
266 plicable for understanding the mechanisms of skeletal patterning along a proximal-distal axis.
267  the salamander limb including regulation of skeletal patterning during epimorphic regeneration, skel
268  glycosaminoglycans storage was reduced, and skeletal phenotype was ameliorated.
269 ling in osteoblasts in vivo, we analyzed the skeletal phenotypes of mice lacking these receptors in o
270 n studies; (2) gene-function prediction; (3) skeletal phenotyping of 120 knockout mice with deletions
271 on, suggesting differences in patterning and skeletal regeneration.
272 e identified that in disease-free bones this skeletal region contained smaller and less-oriented HA n
273 d the proportion of patients with at least 1 skeletal-related event by disease type, pain as assessed
274  12-week dosing group experienced at least 1 skeletal-related event within 2 years of randomization (
275                                      Purpose Skeletal-related events (SREs) such as pathologic fractu
276 minobisphosphonate, reduces the incidence of skeletal-related events and pain in patients with bone m
277 ion, skeletal morbidity rate (mean number of skeletal-related events per year), and, in a subset of 5
278 icrobiota's osteoimmunomodulatory effects on skeletal remodeling and homeostasis are unclear in the h
279 t (KO) alters the single-channel function of skeletal RyR (RyR1).
280 e, appendicular lean soft tissue, and WB and skeletal site-specific BMC acquisition and to measure th
281 ssess the acquisition of whole-body (WB) and skeletal site-specific bone mineral content (BMC) relati
282 ng approach could be easily applied to other skeletal sites and transgenic models, and could improve
283     Collectively, these results suggest that skeletal sites prone to tumor cell dissemination contain
284                                          The skeletal sites showing the greatest abnormality in the c
285     These findings provide insights into how skeletal stem and progenitor cells interact with other c
286 ur findings further the understanding of the skeletal stem/progenitor cells in adult life.
287                  Proper bone homeostasis and skeletal strength are maintained by balancing OC functio
288 ently to collectively re-form a now branched skeletal structure.
289  the maxilla to the mandible) seem to be the skeletal subspaces that receive the main effect of the t
290 r achieving specific functions, ranging from skeletal support to mastication, from sensors and defens
291 pment and function of the cerebellum and the skeletal system.
292 ro-mechanical interplay in the neuro-musculo-skeletal system.
293 a close interrelationship between immune and skeletal systems and suggests an osteolytic role of IL-1
294 hanced activation of the cardiac TF over the skeletal TF by Ca(2+) and lead to a mechanistic model fo
295 l patterning during epimorphic regeneration, skeletal tissue differentiation during regeneration, and
296 to sensory nerves that innervate the bone or skeletal tissue has not been shown.
297 ctor is controversial and remains unknown in skeletal tissues.
298                            The appearance of skeletal traits related to endurance (e.g., larger limb
299 stic value of the quantitative assessment of skeletal tumor burden on bone scintigraphy (Bone Scan In
300 scellaneous structures based on 54 different skeletal types.

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