ライフサイエンスコーパス: hypofunction

1 frequency and N-methyl-D-aspartate receptor hypofunction.

2 d (SG) and result in the associated salivary hypofunction.

3 tients with unilateral peripheral vestibular hypofunction.

4 with vagal hyperreactivity rather than vagal hypofunction.

5 otypes in the genetic model of NMDA receptor hypofunction.

6 ction in schizophrenia is secondary to NMDAR hypofunction.

7 rom one side to induce unilateral mandibular hypofunction.

8 al aberrations associated with NMDA receptor hypofunction.

9 d D-serine and N-methyl-D-aspartate receptor hypofunction.

10 eurodevelopmental deficit, and glutamatergic hypofunction.

11 RG1/erbB4 signaling leading to glutamatergic hypofunction.

12 e for disorders characterized by cholinergic hypofunction.

13 ns of residues 316 or 317 would predict MC4R hypofunction.

14 ics to treat disorders associated with NMDAR hypofunction.

15 er in elderly men may be related to HPG axis hypofunction.

16 rmal levels could be used to define salivary hypofunction.

17 ow rates over 6 hours and to define salivary hypofunction.

18 for the treatment of postradiation salivary hypofunction.

19 g or disorders characterized by dopaminergic hypofunction.

20 gland immune cell infiltration and glandular hypofunction.

21 ction in diseases that feature NMDA receptor hypofunction.

22 reclinical models characterized by GABAergic hypofunction.

23 pathological cells but also as one of immune hypofunction.

24 confirmed unilateral or bilateral vestibular hypofunction.

25 rupts acinar polarity, resulting in salivary hypofunction.

26 its, revealing sex-specific effects of EPHB2 hypofunction.

27 ulation of aggression in BALB/cJ mice to ACC hypofunction.

28 increased GABA decay times and NMDA receptor hypofunction.

29 rial function contributing to salivary gland hypofunction.

30 nsistent with cumulative mesolimbic dopamine hypofunction.

31 ted by pharmaceutical treatments for thyroid hypofunction.

32 ers in early trials addressing NMDA receptor hypofunction.

33 ESI-potentiated heroin-seeking and neuronal hypofunction.

34 syndrome-like features, suggesting p110alpha hypofunction.

35 increased neural excitability, and astrocyte hypofunction.

36 therapy against irradiation-induced salivary hypofunction.

37 tion as a treatment for bilateral vestibular hypofunction.

38 ethyl-D-aspartate glutamate receptor (NMDAR) hypofunction.

39 damage was required for both senescence and hypofunction.

40 growth retardation due to placental vascular hypofunction.

41 schizophrenia genetic risk and NMDA receptor hypofunction.

42 working memory deficits associated with NMDA hypofunction.

43 onstrating inflammation-induced serotonergic hypofunction.

44 order characterized by NMDAR and cholinergic hypofunctions.

45 hic support by NGF to ameliorate cholinergic hypofunctioning.

46 iness (14 [22.6%]), or unilateral peripheral hypofunction (9 [14.5%]).

47 pathway, dopamine hyperfunction and/or NMDA hypofunction abnormalities implicated in schizophrenia m

48 To better understand how NMDAR hypofunction affects the brain, we used magnetic resonan

49 te increase in dopamine release (followed by hypofunction after chronic use) and cue exposure-induced

50 each of humoral self-tolerance, and salivary hypofunction after delivery of a replication-deficient a

51 hat exceed those caused by NMDAR interneuron hypofunction alone.SIGNIFICANCE STATEMENT NMDAR hypofunc

52 tural phase signaling, whereas NMDA receptor hypofunction alters interstructural and intrastructural

53 two common vestibular disorders - vestibular hypofunction and benign paroxysmal positional vertigo (B

54 Furthermore, hypofunction and BMP-2 increase the development of trans

55 ongenital sensorineural deafness, vestibular hypofunction and childhood onset retinitis pigmentosa.

56 While this demonstrates causality between MD hypofunction and cognitive inflexibility, questions rema

57 iodine deficiency and mild maternal thyroid hypofunction and decreased child cognition.

58 action similarly reduced the impact of NMDA hypofunction and dopamine hyperfunction on OFC neurons,

59 erferon (IFN) alfa for treatment of salivary hypofunction and dry mouth symptoms in primary Sjogren's

60 Symptoms of both HPG axis hypofunction and dysthymic disorder include dysphoria, f

61 ate network alterations may arise from NMDAR hypofunction and establish a proof of principle whereby

62 Treatments for unilateral vestibular hypofunction and for posterior canal BPPV are effective;

63 Thus, developmental NMDAR hypofunction and glutathione system deficits, separately

64 clinical consequences of maternal CD8 T cell hypofunction and identify pregnancy as a previously unap

65 Prefrontal localized hypofunction and impaired serotonergic responsivity are

66 nt's disease is a direct consequence of CLC5 hypofunction and is not attributable to a gain of functi

67 and female primates that aHipp glutamatergic hypofunction and its regulation by area 25 contribute to

68 endrocyte differentiation, and interneuronal hypofunction and network imbalance emerged after 3 days,

69 due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin (PV) neuronal dysfunction l

70 Vagal hypofunction and prolonged intra-esophageal acidificatio

71 ism may be mechanisms driving reward network hypofunction and RR deficits.

72 rong positive association between testicular hypofunction and subsequent MS (rate ratio = 4.62, 95% c

73 ted levels of KYNA could contribute to NMDAR hypofunction and the cognitive deficits and negative sym

74 t Lnx1 deletion causes NMDA receptor (NMDAR) hypofunction and this is attributable to decreased GluN2

75 ossible to reduce the risk of salivary gland hypofunction and xerostomia.

76 For the prevention of salivary gland hypofunction and/or xerostomia in patients with head and

77 For the management of salivary gland hypofunction and/or xerostomia, intermediate-quality evi

78 For patients who develop salivary gland hypofunction and/or xerostomia, interventions include to

79 tinction of aged animals may relate to NMDAR hypofunctioning and a lack of NMDAR-dependent LTD.

80 e, decreased susceptibility to tumor-induced hypofunction, and attenuation of IR expression compared

81 nk among chronic stress, prefrontal cortical hypofunction, and behavioral dysfunction.

82 c links between early-life stress, astrocyte hypofunction, and behavioural deficits.

83 ogy could be linked to NMDA receptor (NMDAR) hypofunction, and thus used the serine racemase-null mut

84 prevalence of xerostomia and salivary gland hypofunction appears to be significantly higher in HIV-p

85 adult mutants, adrenocortical dysplasia and hypofunction are predominant features.

86 te strong evidence for NMDA receptor (NMDAR) hypofunction as an underlying factor for cognitive disor

87 d a potential association between testicular hypofunction, as a proxy for low testosterone levels, an

88 R function and could compensate for receptor hypofunction associated with certain neuropsychiatric di

89 nvolved in the development of salivary gland hypofunction associated with SjD.

90 unction precedes the hippocampal cholinergic hypofunction associated with structural cholinergic dege

91 for many patients with bilateral vestibular hypofunction (BVH).

92 suggest that Shank3 deficiency induces NMDAR hypofunction by interfering with the Rac1/PAK/cofilin/ac

93 uced hippocampal ACh release and cholinergic hypofunction by selective impairment of desensitization

94 ndrome of dRTA and hemolytic anemia in which hypofunction can be discerned by in vitro studies.

95 These results demonstrate that NMDAR hypofunction can reproduce the numerous hippocampal defi

96 on remained unimpaired at the level of GluN1-hypofunction caused by our manipulation.

97 Mediodorsal thalamus hypofunction causes cognitive inflexibility reflected by

98 ion, SRKO mice demonstrate how chronic NMDAR hypofunction contributes to deficits in certain translat

99 Cholinergic hypofunction contributes to dementia-related cognitive d

100 stantial evidence that NMDA receptor (NMDAR) hypofunction contributes to the pathophysiology of schiz

101 lation, SAPK/JNK activation, and proteasomal hypofunction cooperate to produce further protein accumu

102 litus (DM2), these findings suggest that IDE hypofunction could mediate human disease.

103 These results indicate that NMDAR hypofunction critically contributes to FTD-associated be

104 sly reported molecular underpinnings of GluN hypofunction (decreased GluN2 phosphorylation) and here

105 To establish whether IDE hypofunction decreases Abeta and insulin degradation in

106 le Pavlovian learning was not affected by MD hypofunction, decreasing MD activity during Pavlovian le

107 a potential target for treatment of salivary hypofunction diseases.

108 strate that a genetic model of NMDA receptor hypofunction displays a reduced ability to extinguish co

109 ns such as why some patients with vestibular hypofunction do not improve with a course of vestibular

110 individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with

111 ds lead to Rome" hypothesis, i.e., how NMDAR hypofunction during development acts as a convergence po

112 We show that transient NMDAR hypofunction during early brain development, coinciding

113 s that metabolic insufficiency drives T cell hypofunction during tonic stimulation, but the signals t

114 Patients with salivary hypofunction exhibit difficulty in chewing and swallowin

115 The modest degree of hypofunction exhibited in vitro by these mutations, howe

116 opathic (1 participant) bilateral vestibular hypofunction for 2 to 23 years underwent unilateral impl

117 us-host disease (GVHD), implying endothelial hypofunctioning for thrombomodulin-dependent generation

118 t out the pathological relevance of GSK3beta hypofunction found in humans and contribute to understan

119 lular-level abnormalities--eg, NMDA receptor hypofunction, GABA system dysfunction, neural connectivi

120 We tested the hypothesis that hypofunction has a greater influence than ovariectomy on

121 NMDAR hypofunction has been implicated in schizophrenia becaus

122 pact on NMDA receptors (NMDARs), since NMDAR hypofunction has been implicated in schizophrenia.

123 N-methyl-D-aspartate receptor (NMDAR) hypofunction has been implicated in several neurodevelop

124 ogical treatment of disorders in which NMDAR hypofunction has been implicated.

125 N-Methyl-D-aspartate (NMDA) receptor (NMDAR) hypofunction has been postulated to contribute to the co

126 cularly N-methyl-D-aspartate (NMDA) receptor hypofunction, has long been postulated to be part of the

127 chizophrenia, that result from NMDA receptor-hypofunction have been mainly attributed to dysfunction

128 phrenia-1 (DISC1) and D-serine/NMDA receptor hypofunction have both been implicated in the pathophysi

129 ion and experimental models of NMDA receptor hypofunction have proven useful for characterizing neuro

130 hyperactivity, N-methyl-d-aspartate receptor hypofunction, hippocampal hyperactivity, immune dysregul

131 The NMDA receptor (NMDAR) hypofunction hypothesis of schizophrenia is supported by

132 ies and form the basis for the NMDA receptor hypofunction hypothesis of SZ.

133 have witnessed a rise in the 'NMDA receptor hypofunction' hypothesis for schizophrenia, a devastatin

134 n proposed as a model for the intrinsic NMDA hypofunction hypothesized for schizophrenia.

135 While MD hypofunction impaired reversal learning, it did not affe

136 ary for set-shifting, and that NMDA receptor hypofunction impairs the capacity to modify existing kno

137 ssociated with xerostomia and salivary gland hypofunction in a population of HIV-positive women.

138 T and may act, in part, by normalizing daMCC hypofunction in ADHD.

139 litis supports a hypothesis of glutamatergic hypofunction in catatonia.

140 ofunction alone.SIGNIFICANCE STATEMENT NMDAR hypofunction in cortical interneurons has been linked to

141 ystemic inflammation and chronic cholinergic hypofunction in delirium and have implications for the r

142 However, to what extent NMDAR-hypofunction in distinct cell-types across the brain cau

143 of schizophrenia by promoting NMDA receptor hypofunction in fast-spiking interneurons.

144 The etiology of salivary gland hypofunction in HIV(+) patients is unclear.

145 We have transiently induced NMDAR hypofunction in infant mice during postnatal days 7-11,

146 nd their predictions in the context of NMDAR hypofunction in INs.

147 -DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

148 -DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

149 MEF2C hypofunction in neurons is presumed to underlie most of

150 s, we also discuss the implications of NMDAR hypofunction in other types of INs using computational m

151 N-methyl-D-aspartate receptor (NMDAR) hypofunction in parvalbumin-expressing (PV+) inhibitory

152 rugs for alleviating symptoms of cholinergic hypofunction in patients with advanced Alzheimer's disea

153 However, if NMDAR-hypofunction in prefrontal excitatory neurons may indeed

154 However, it remains to be seen if NMDAR hypofunction in PV+ neurons is fundamental to the phenot

155 ta demonstrate for the first time that NMDAR hypofunction in pyramidal cells is sufficient to cause e

156 NMDA receptor hypofunction in schizophrenia has been inferred by a lar

157 hanced NRG1 signaling may contribute to NMDA hypofunction in schizophrenia.

158 al role in the development of salivary gland hypofunction in SjD by promoting endolysosomal degradati

159 No conventional therapy exists for salivary hypofunction in surviving head and neck cancer patients

160 Repeated injections of alloantigens drove hypofunction in TEa cells and rendered grafts resistant

161 The findings suggest hypofunction in the anterior cingulate cortex in schizop

162 The neonatal sensitivity to NMDA receptor hypofunction in the BSTC, and in its main thalamic targe

163 ics and brain imaging implicate dopaminergic hypofunction in the frontal lobes and basal ganglia in A

164 ressive disorders, as well as neural circuit hypofunction in the medial prefrontal cortex (mPFC).

165 of type III Nrg1 heterozygous mice revealed hypofunction in the medial prefrontal cortex and the hip

166 The results suggest that the NMDA receptor hypofunction in the NR1 -/- mice is not global but regio

167 ical and clinical studies implicate dopamine hypofunction in the pathophysiology of depression.

168 ansmission and N-methyl-D-aspartate receptor hypofunction in the pathophysiology of psychotic disorde

169 ated with cognitive dysfunction and dopamine hypofunction in the prefrontal cortex, particularly schi

170 macological demonstration that glutamatergic hypofunction in the ventral hippocampus lies at the core

171 ch is associated with adult serotonin system hypofunction in the ventral hippocampus.

172 owever the neurochemistry underlying network hypofunction in those with low RR remains unclear.

173 ur findings provide evidence for overlapping hypofunction in ventral striatal and orbitofrontal regio

174 subset of transcripts vulnerable to Pol III hypofunction, including a global reduction in tRNA level

175 bute to core symptoms arising from glutamate hypofunction, including cognitive impairments.

176 results suggest that 8-OH-DPAT-induced 5-HT hypofunction increases thirst without substantially affe

177 nditions and during a state of relative NMDA hypofunction induced by ketamine administration, at a do

178 Bilateral vestibular hypofunction is associated with chronic disequilibrium,

179 are suggestions in the literature that glial hypofunction is associated with depressive symptoms and

180 Salivary hypofunction is associated with oral and pharyngeal diso

181 ergic interneuron deficits and NMDA receptor hypofunction is associated with the hyperdopaminergic st

182 showed that in female rats with DM, salivary hypofunction is correlated with decreased submandibular

183 GABAergic interneuron hypofunction is hypothesized to underlie hippocampal dys

184 NMDA-receptor (NMDAR) hypofunction is strongly implicated in the pathophysiolo

185 One strategy to correct NMDAR hypofunction is to stimulate alpha-amino-3-hydroxy-5-met

186 efrontal cortex (PFC), but the origin of the hypofunction is unclear.

187 milar mechanism of NMDAR-mediated inhibitory hypofunction leading to cortical disinhibition has been

188 Hypofunction led to alveolar bone becoming more highly m

189 t the disruption of circuit function by Pten hypofunction may be ongoing well beyond early developmen

190 dingly, experimental models of NMDA receptor hypofunction may be useful for testing potential new ant

191 ggesting a possible mechanism by which EPHB2 hypofunction may contribute to sex-specific motor-relate

192 NMDA receptor hypofunction may contribute to the comorbidity of substa

193 h the hypothesis that thalamic glutamatergic hypofunction may contribute to the pathophysiology of th

194 Instead, maternal thyroid hypofunction may serve as a proxy indicator for other fa

195 dence, our in vivo findings suggest that IDE hypofunction may underlie or contribute to some forms of

196 D-aspartate receptor (NMDAR) development and hypofunction, may lead to the dysfunction of both local

197 stibular prosthesis for bilateral vestibular hypofunction, measures of posture, gait, and quality of

198 ment of new antipsychotics based on the NMDA hypofunction model for schizophrenia.

199 The N-methyl-d-aspartic acid receptor hypofunction model of schizophrenia predicts a paradoxic

200 The N-methyl-D-aspartate receptor hypofunction model of schizophrenia predicts dysfunction

201 lices using the N-methyl-D-asparate receptor hypofunction model show that delta frequency bursting is

202 ted by the N-methyl-d-aspartic acid receptor hypofunction model.

203 Notably, gene expression induced during TIL hypofunction more closely resembled self-tolerance than

204 utyric acid-ergic interneuron-specific NMDAR hypofunction mouse model (Ppp1r2-Cre/fGluN1 knockout [KO

205 velopment programs that target NMDA receptor hypofunction, neuroimaging results play a critical role

206 imer's disease (AD) is marked by cholinergic hypofunction, neuronal marker loss, and decreased nicoti

207 mice with genetically induced NMDA receptor hypofunction [NMDA receptor subunit-1 knockdown (NR1-KD)

208 l object recognition memory in NMDA receptor hypofunctioning NR1-knockdown mice, and were essentially

209 In addition, an NMDA receptor hypofunction (NRHypo) state may play a role in neurodege

210 Consistent with NMDA-mediated hypofunction observed in schizophrenic subjects, adminis

211 ging theory of schizophrenia postulates that hypofunction of adenosine signaling may contribute to it

212 Upregulation of NMDARs might contribute to hypofunction of AMPARs via subcellular redistribution.

213 gnized dependence of hypermutated tumours on hypofunction of genes that are involved in chromatin rem

214 ing coagonist D-serine was able to attenuate hypofunction of GluN2B(p.P553T)-containing NMDARs.

215 ic patients, exhibit behavioral deficits and hypofunction of glutamatergic and GABAergic pathways.

216 est that decreased outward K(+) current from hypofunction of Kir2.6 predisposes the sarcolemma to hyp

217 As hypofunction of N-methyl-d-aspartate (NMDA) receptor-dri

218 Hypofunction of N-methyl-d-aspartate (NMDA) receptors ha

219 the early 1990s it has been postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in

220 A hypofunction of N-methyl-D-aspartate glutamate receptors

221 bit behavioral abnormalities consistent with hypofunction of NMDA neurotransmission.

222 Schizophrenia may involve hypofunction of NMDA receptor (NMDAR)-mediated signaling

223 in schizophrenia, which is characterized by hypofunction of NMDA receptor (NMDAR)-mediated transmiss

224 This experimental design models the proposed hypofunction of NMDA receptor and gamma-aminobutyric aci

225 cal theories of schizophrenia emphasize that hypofunction of NMDA receptors at critical sites in loca

226 Hypofunction of NMDA receptors has been considered a pos

227 uced AMPAR-GluA2/3 in the entorhinal cortex, hypofunction of NMDAR in cortical areas, and a decrease

228 c agents directed toward diseases related to hypofunction of NMDAR.

229 Our data suggest that a hypofunction of NMDARs in prefrontal excitatory neurons

230 ow dopaminergic activation induces long-term hypofunction of NMDARs, which can contribute to disorder

231 rtical synaptic transmission at two sites: a hypofunction of postsynaptic NMDA receptors, and by redu

232 Irreversible hypofunction of salivary glands is a common side effect

233 eck cancers frequently leads to irreversible hypofunction of salivary glands, which severely compromi

234 These results provide direct evidence that hypofunction of striatal FSIs can produce movement abnor

235 ominant-negative SNARE expression leads to a hypofunction of synaptic NMDARs, we conclude that astroc

236 he prevailing models of schizophrenia invoke hypofunction of the glutamatergic synapse and defects in

237 and PET/SPECT studies support the theory of hypofunction of the N-methyl-D-aspartate receptor (NMDAR

238 rimarily to chloride dysregulation caused by hypofunction of the potassium-chloride co-transporter KC

239 that this behavior involves cocaine-induced hypofunction of the prefrontal cortex (PFC) or "hypofron

240 n schizophrenia are thought to derive from a hypofunction of the prefrontal cortex (PFC), but the ori

241 Hypofunction of the serotonergic system is often associa

242 ce that traumatic brain injury (TBI) induces hypofunction of the striatal dopaminergic system, the me

243 Hypofunctioning of a specific orbitofrontal cortical net

244 d that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-aminobutyric acid (GABA) interneur

245 espect to magnitude and dependency of T cell hypofunction on NFAT-independent signals.

246 chotic efficacy, reversed the impact of NMDA hypofunction on OFC cells and on behavior.

247 ehaviour, we simulated the effects of NMDA-R hypofunction onto either excitatory or inhibitory neuron

248 on the treatment of patients with vestibular hypofunction or with benign paroxysmal positional vertig

249 , 28% to 42%]) and those with salivary gland hypofunction (OR, 3.02 [95% CI, 1.73 to 5.28]).

250 tivity contributes to organ failure, whereas hypofunction permits sepsis.

251 ggests N-methyl-D-aspartate receptor (NMDAR) hypofunction plays a central role in the pathophysiology

252 N-methyl-D-aspartate receptor (NMDA-R) hypofunction plays an important role in cognitive impair

253 o impairing cognition that occurs with NMDAR hypofunction, potentially tied to impaired task-dependen

254 mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Grin1 knockout mice).

255 Because this nonstructural cholinergic hypofunction precedes the hippocampal cholinergic hypofu

256 al excitation/inhibition balance from NMDA-R hypofunction predominantly onto excitatory neurons.

257 However, KCC2 hypofunction promotes mechanical pain hypersensitivity i

258 tal disorders characterized by NMDA receptor-hypofunction.Proper brain function depends on the correc

259 induced in the N-methyl-D-asparate receptor hypofunction rat model.

260 e in primates that hippocampal glutamatergic hypofunction regulates endogenous high-trait anxiety and

261 l alterations that results from serotonergic hypofunction remain poorly understood.

262 istent with the theory that individuals with hypofunctioning reward circuitry overeat to compensate f

263 Significant associations between a hypofunctioning reward response and obesity suggest the

264 in osteocyte density in alveolar bone, while hypofunction showed an increase compared with controls.

265 blished, but factors that underlie secretory hypofunction, specifically related to the autoimmune dis

266 a disorder repeatedly associated with NMDAR hypofunction, spend more time in the external mode.

267 -dependent NMDA antagonist to model the NMDA hypofunction state that may occur in schizophrenia.

268 Conclusions: Results suggest hypofunction stimulates early bone formation.

269 Previous studies have reported hypofunction, structural abnormalities, and biochemical

270 rebrain and to model diseases of cholinergic hypofunction such as Alzheimer's disease.

271 ss lifetime risks of infertility, testicular hypofunction, testicular atrophy, and a composite of low

272 n NR1 phosphorylation leads to glutamatergic hypofunction that can contribute to behavioral deficits

273 is not necessarily accompanied by the DLPFC hypofunction that was seen in schizophrenia.

274 reveal the importance of aHipp glutamatergic hypofunction, the causal involvement of aHipp glutamate

275 Consistent with the NMDAR hypofunction theory of schizophrenia, distinct schizophr

276 s about the mechanisms that might link NMDAR hypofunction to alterations of FS neurons in schizophren

277 a mouse model of radiation-induced salivary hypofunction to investigate the outcomes of DNA damage i

278 hat is overtly symptomatic, and link torsinA hypofunction to neurodegeneration and abnormal twisting

279 ent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophre

280 a dystonic motor phenotype and link torsinA hypofunction to the development of early neuropathologic

281 t link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiology of schizophrenia.

282 test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects

283 us, consistent with the hypothesis that GABA hypofunction underlies the pathophysiology of the disord

284 us, consistent with the hypothesis that GABA hypofunction underlies the pathophysiology of the disord

285 prevented both senescence and salivary gland hypofunction via a mechanism involving enhanced DNA dama

286 from SjD patients showed that salivary gland hypofunction was associated with decreased expression of

287 Results indicated that maternal thyroid hypofunction was associated with progeny ADHD but possib

288 Recently, NMDA receptor hypofunction was described in patients with psychotic ma

289 This platelet hypofunction was reversible and associated with purinerg

290 y a role in clinical cases of salivary gland hypofunction, we developed an aquaporin 5 (AQP5) Cre mou

291 Using a pharmacogenetic approach to model MD hypofunction, we recently showed that decreasing MD acti

292 and neck cancer is persistent salivary gland hypofunction which causes xerostomia and oral infections

293 gs support the hypothesis that NMDA receptor hypofunction, which has been implicated in the pathophys

294 cy in forebrain or PFC induces NMDA receptor hypofunction, while Cul3 loss in striatum causes a cell

295 Salivary gland fibrosis results in salivary hypofunction whose current treatments are palliative.

296 ing radiotherapy leads to severe and chronic hypofunction with decreased salivary output, xerostomia,

297 une sialadenitis resulting in salivary gland hypofunction with dry mouth symptom.

298 association of xerostomia and salivary gland hypofunction with HIV infection has been established for

299 t the common variant exists on a spectrum of hypofunction with potential for reversibility.

300 autism, our data raise the possibility that hypofunction within this meta-circuit is a shared featur