Characterization of the colostrum and transition milk proteomes from primiparous and multiparous Holstein dairy cows.

Colostrum plays a vital role in the nutrition, development, and immunity of a newborn calf. This study aimed to characterize the protein profile of colostrum and to identify changes in the colostrum proteome across parity during the transition to mature milk. Colostrum and transition milk samples were collected at milkings 1, 2, 4, and 14 after calving from multiparous (n = 10) and primiparous cows (n = 10). Samples were skimmed, fractionated, and enriched before analysis for low-abundance proteins by liquid chromatography-tandem mass spectroscopy (LC-MS/MS). Changes in protein abundances were analyzed using PROC MIXED in SAS (SAS Institute Inc., Cary, NC) with determination of the adaptive false discovery rate adjustment using a MULTTEST procedure to identify effects of parity (P), milking number (MN), and their interaction (MN×P). We identified 86 proteins through LC-MS/MS, including 3 low-abundance proteins that were affected by P, 78 that were affected by MN, and 36 affected by MN×P. Prominent ontological groupings of proteins affected by MN included defense or immunity proteins, such as immunoglobulins. Proteins involved in the plasminogen activating cascade and more broadly, blood coagulation, were affected by MN×P. The results of this study add to increasing knowledge of the colostrum and transition milk proteomes, and this is the first study to find evidence of different abundances of these proteins when examined across P, MN, and MN×P. These findings aid in the identification of potential milk protein biomarkers for mammary health during the early postpartum period.

Altered mucosa-associated microbiota in the ileum and colon of neonatal calves in response to delayed first colostrum feeding.

The present study investigated whether delaying the first feeding of colostrum affected ileum and colon mucosa-associated microbiota in calves. Twenty-seven male Holstein calves were randomly assigned to 1 of 3 groups, fed colostrum at 45 min, 6 h, and 12 h after birth, respectively. Ileum and colon mucosa were collected at 51 h after birth, and their associated microbial profiles were assessed using amplicon sequencing. Both ileum and colon mucosa-associated microbiota were predominated by genus Escherichia-Shigella. The negative correlation between the molar proportion of short-chain fatty acids (SCFA) and ileum mucosa-associated opportunistic pathogens, and the positive correlation between the molar proportion of SCFA and colon mucosa-associated beneficial bacteria, suggest that SCFA might play an important role in maintaining the gut health of 2-d-old calves. A higher relative abundance of ileum mucosa-associated Enterococcus and Streptococcus was detected when the first colostrum feeding was delayed for 12 h. The relative abundance of colon mucosa-associated Lactobacillus tended to be lower in calves fed colostrum 12 h than those under the other 2 treatments, whereas that of Faecalibacterium tended to be lower in calves fed colostrum immediately after birth than those fed colostrum 6 and 12 h after birth, respectively. Our findings suggest that delayed first colostrum feeding affects the establishment of ileum and colon mucosa-associated bacteria, which may have long-term effects on gut health of calves.

Effect of delaying colostrum feeding on passive transfer and intestinal bacterial colonization in neonatal male Holstein calves.

The objective of this study was to investigate the effect of time of first colostrum feeding on the passive transfer of IgG and on bacterial colonization in the intestine of neonatal dairy calves. Twenty-seven male Holstein calves were randomly assigned to 1 of 3 treatments at birth: calves were fed colostrum at 45 min (0 h, n = 9), 6 h (n = 9), or 12 h after birth (n = 9). Calves were fed pooled, heat-treated colostrum (62 g of IgG/L) at their respective feeding times at 7.5% of birth body weight and fed milk replacer at 2.5% of birth body weight per meal every 6 h thereafter. Blood samples were taken every 3 h using a jugular catheter and were analyzed for determination of serum IgG by radial immunodiffusion. At 51 h after birth, calves were euthanized for collection of tissue and digesta of the distal jejunum, ileum, and colon. Quantitative real-time PCR was used to estimate the prevalence of Bifidobacterium spp., Lactobacillus spp., Fecalibacterium prausnitzii, Clostridium cluster XIVa, and total Escherichia coli. Delaying colostrum feeding by 6 h (35.6 ± 1.88%) and 12 h (35.1 ± 3.15%) decreased the maximum apparent efficiency of absorption of IgG compared with feeding colostrum immediately after birth (51.8 ± 4.18%) and delayed the time to maximum serum IgG concentration (24 h vs. 15 h, respectively). Moreover, 12-h calves tended to have a lower prevalence of Bifidobacterium spp. (0.12 ± 0.017%) and Lactobacillus spp. (0.07 ± 0.019%) associated with the colon mucosa compared with 0-h calves (1.24 ± 0.648% and 0.26 ± 0.075%, respectively). In addition, 6-h (0.26 ± 0.124%) and 12-h (0.49 ± 0.233%) calves had a lower prevalence of total E. coli associated with ileum mucosa compared with 0-h calves (1.20 ± 0.458%). These findings suggest that delaying colostrum feeding within 12 h of life decreases the passive transfer of IgG and may delay the colonization of bacteria in the intestine, possibly leaving the calf vulnerable to infections during the preweaning period.

Systemic gene delivery transduces the enteric nervous system of guinea pigs and cynomolgus macaques.

Characterization of adeno-associated viral vector (AAV) mediated gene delivery to the enteric nervous system (ENS) was recently described in mice and rats. In these proof-of-concept experiments, we show that intravenous injections of clinically relevant AAVs can transduce the ENS in guinea pigs and non-human primates. Neonatal guinea pigs were given intravenous injections of either AAV8 or AAV9 vectors that contained a green fluorescent protein (GFP) expression cassette or phosphate-buffered saline. Piglets were euthanized three weeks post injection and tissues were harvested for immunofluorescent analysis. GFP expression was detected in myenteric and submucosal neurons along the length of the gastrointestinal tract in AAV8 injected guinea pigs. GFP-positive neurons were found in dorsal motor nucleus of the vagus and dorsal root ganglia. Less transduction occurred in AAV9-treated tissues. Gastrointestinal tissues were analyzed from young cynomolgus macaques that received systemic injection of AAV9 GFP. GFP expression was detected in myenteric neurons of the stomach, small and large intestine. These data demonstrate that ENS gene delivery translates to larger species. This work develops tools for the field of neurogastroenterology to explore gut physiology and anatomy using emerging technologies such as optogenetics and gene editing. It also provides a basis to develop novel therapies for chronic gut disorders.

The appraisal of public health interventions: an overview.

BACKGROUND: The approach currently used to appraise public health interventions is close to that of health technology appraisal for drugs. This approach is not appropriate for many public health interventions, however, when extremely small individual level benefits are delivered to extremely large populations. In many such situations, randomized controlled trials with sufficient size and power to determine individual level effects are impractical. Such interventions may be cost-effective, even in the absence of traditional evidence to demonstrate this. METHODS: We outline an alternative approach based on decision theory. We apply it to cases where prior beliefs are sufficiently strong and well grounded to allow decision-makers to assume the direction of change of the intervention's outcome, within the context of a transparent and deliberative decision-making process. Decision theory also assumes that decision-makers are risk neutral, implying that they should make decisions based on an intervention's mean cost-effectiveness, and should therefore disregard variance except when deciding to wait for more information. However, they must allow for biases. RESULTS: A framework is presented which has the potential to achieve large health gains at no additional cost. CONCLUSIONS: This analysis provides a rigorous theoretical framework for decision-makers in public health. The implied paradigm shift also applies to some clinically based areas.

AAV retinal transduction in a large animal model species: comparison of a self-complementary AAV2/5 with a single-stranded AAV2/5 vector.

PURPOSE: To compare self-complementary (sc) and single-stranded (ss) adeno-associated viral 2/5 (AAV2/5) vectors for retinal cell transduction in the dog when delivered by subretinal injection. METHODS: ScAAV2/5 and ssAAV2/5 vectors encoding enhanced green fluorescent protein (GFP) under control of the chicken beta actin promoter were prepared to the same titer. Equal amounts of viral particles were delivered into the subretinal spaces of both eyes of two dogs. In each dog, one eye received the scAAV2/5 and the other the ssAAV2/5. In vivo expression of GFP was monitored ophthalmoscopically. The dogs were sacrificed, and their retinas were examined by fluorescent microscopy and immunohistochemistry to determine GFP expression patterns and to assay for glial reactivity. RESULTS: GFP expression in the scAAV2/5 injected eyes was detectable at a much earlier time point than in the ssAAV2/5 injected eyes. Expression of GFP was also at higher levels in the scAAV2/5-injected eyes. Expression levels remained stable for the seven month duration of the study. The types of cells transduced by both vectors were similar; there was strong reporter gene expression in the RPE and photoreceptors, although not all cones in the transduced area expressed GFP. Some horizontal and Müller cells were also transduced. CONCLUSIONS: When delivered by subretinal injection in the dog, scAAV2/5 induces faster and stronger transgene expression than ssAAV2/5. The spectrum of retinal neurons transduced is similar between the two vectors. These results confirm in a large animal model those previously reported in the mouse. ScAAV2/5 shows promise for use in the treatment of conditions where a rapid transgene expression is desirable. Furthermore, it may be possible to use a lower number of viral particles to achieve the same effect compared with ssAAV2/5 vectors.

Müller glia are a potential source of neural regeneration in the postnatal chicken retina.

The retina of warm-blooded vertebrates is believed to be incapable of neural regeneration. Here we provide evidence that the retina of postnatal chickens has the potential to generate new neurons. In response to acute damage, numerous Müller glia re-entered the cell cycle, and shortly thereafter, expressed CASH-1, Pax6 and Chx10, transcription factors expressed by embryonic retinal progenitors. These progenitor-like cells transiently expressed neurofilament. Newly formed cells became distributed throughout the inner and outer nuclear layers of the retina, and remained for at least three weeks after damage. Some of these newly formed cells differentiated into retinal neurons, a few formed Müller glia, and most remained undifferentiated, with continued expression of Pax6 and Chx10. These cells continued to proliferate when grown in culture, with some differentiating into retinal neurons or Müller glia. We propose that, in response to damage, Müller glia in the retina are a potential source of neural regeneration.

Light- and focus-dependent expression of the transcription factor ZENK in the chick retina.

Ocular growth and refraction are regulated by visual processing in the retina. We identified candidate regulatory neurons by immunocytochemistry for immediate-early gene products, ZENK (zif268, Egr-1) and Fos, after appropriate visual stimulation. ZENK synthesis was enhanced by conditions that suppress ocular elongation (plus defocus, termination of form deprivation) and suppressed by conditions that enhance ocular elongation (minus defocus, form deprivation), particularly in glucagon-containing amacrine cells. Fos synthesis was enhanced by termination of visual deprivation, but not by defocus and not in glucagon-containing amacrine cells. We conclude that glucagon-containing amacrine cells respond differentially to the sign of defocus and may mediate lens-induced changes in ocular growth and refraction.

Late watergrass (Echinochloa phyllopogon): mechanisms involved in the resistance to fenoxaprop-p-ethyl.

Fenoxaprop-p-ethyl (FE), 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy] propanoate, ethyl ester (R), is an aryloxyphenoxypropionate herbicide for postemergence control of annual and perennial grasses in paddy fields; its site of action is acetyl-coenzyme A carboxylase (ACCase), an enzyme in fatty acids biosynthesis. The possible mechanism(s) of resistance to FE in a resistant biotype of Echinochloa phyllopogon was examined, namely, absorption, translocation, and metabolism of FE and ACCase susceptibility to fenoxaprop acid (FA). Studies of the in vitro inhibition of ACCase discounted any differential active site sensitivity as the basis of resistance to FE. There were differences in absorption rates between biotypes from 3 to 48 h after application (HAA). Biotypes did not differ in either the amounts or the rates of FE translocated; 98% of applied [14C]FE remaining in the treated leaf. However, there was a good correlation between the rate of herbicide metabolism and the plant resistance. The R biotype produced 5-fold less FA and approximately 2-fold more nontoxic (polar) metabolites 48 HAA than the S biotype. Moreover, the higher rate of GSH conjugation in the resistant biotype as compared to the susceptible one indicates that GSH and cysteine conjugation is the major mechanism of resistance of the R biotype against FE toxicity.

[Acute pancreatitis in intensive care medicine : Which risk score is useful?] / Akute Pankreatitis in der Intensivmedizin : Welcher Risikoscore ist hilfreich?

INTRODUCTION: Acute pancreatitis is a disease with an increasing incidence in the Western countries associated with a high mortality depending on severity of disease. Etiology is often biliary or due to alcoholism. Incidence of etiology varies between regions depending on risk-factor prevalence. Several risk scores are available to estimate mortality. The aim of the study is to identify the risk factors most relevant for patients being treated for severe acute pancreatitis in an ICU of a tertiary medical center. PATIENTS AND METHODS: The retrospective cohort study included 91 patients (61.2% men, mean age 52 years) with severe acute pancreatitis who were treated between 2002 and 2013 at the medical ICU of a tertiary medical center. Risk factors were identified using COX regression analysis and associations were assessed with the χ2 test. RESULTS: Pulmonary failure necessitating ventilator support, renal failure requiring renal replacement therapy, need for vasopressor therapy, positive blood cultures, and bleeding complications were identified as risk factors for high mortality in severe acute pancreatitis. Low calcium and high lactate levels are independent risk factors for mortality. CONCLUSION: Critically ill patients with severe pancreatitis have high mortality rates that can be estimated using risk scores. Weighting of risk factors may differ depending on region and severity of disease. For patients included in our study, the Ranson Criteria and the APACHE II Score may be most applicable.

Ischemic Left Ventricular Perforation Covered by a Thrombus in a Patient Presenting with Cerebral Ischemia: Importance of Time-Sensitive Performance and Adequate Interpretation of Bedside Transthoracic Echography.

If myocardial infarction remains silent, only clinical signs of complications may unveil its presence. Life-threatening complications include myocardial rupture, thrombus formation, or arterial embolization. In the presented case, a 76-year-old patient was admitted with left-sided hemiparesis. In duplex sonography, a critical stenosis of the right internal carotid artery was identified and initially but retrospectively incorrectly judged as the potential cause for ischemia. During operative thromboendarterectomy, arterial embolism of the right leg occurred coincidentally, more likely pointing towards a cardioembolic origin. Percutaneous interventions remained unsuccessful and local fibrinolysis was applied. Delayed bedside echocardiography by an experienced cardiologist demonstrated a discontinuity of the normal myocardial texture of the left ventricular apex together with an echodense, partly floating structure merely attached by a thin bridge not completely sealing the myocardial defect, accompanied by pericardial effusion. The patient was immediately transferred to emergency cardiac surgery with extirpation of the thrombus, aortocoronary bypass graft placement, and aneurysmectomy. This didactic case reveals decisive structural shortcomings in patient's admission and triage processes and underlines, if performed timely and correctly, the value of transthoracic echocardiography as a noninvasive and cost-effective tool allowing immediate decision-making, which, in this case, led to the correct but almost fatally delayed diagnosis.

Nitric oxide synthase-containing cells in the retina, pigmented epithelium, choroid, and sclera of the chick eye.

Nitric oxide is a nonconventional neurotransmitter that is produced as needed by the enzyme nitric oxide synthase (NOS). NOS has been detected in numerous neural structures, including distinct populations of retinal neurons in a variety of vertebrate species. The purpose of this study was to identify NOS-containing cells in the retina and extraretinal ocular tissues of hatched chicks. NOS was detected in frozen sections by using nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry and antisera to neuronal NOS. In the retina, NADPH-diaphorase and NOS immunolabelling were present in four subtypes of amacrine cells, some ganglion cells, efferent fibers, efferent target cells, and neuronal processes in both plexiform layers, whereas diaphorase alone was detected in photoreceptor ellipsoids and Müller cells. In addition, NADPH-diaphorase and immunoreactive NOS were detected in axon bundles and innervation to vascular smooth muscle in the choroid, whereas stromal and endothelial cells in the choroid, scleral chondrocytes, and the retinal pigmented epithelium contained only NADPH-diaphorase. The excitotoxin quisqualate destroyed all but one subtype of NOS-immunoreactive amacrine cell and caused increased NADPH-diaphorase activity in Müller cells. We conclude that nitric oxide is produced by many different cells in the chick eye, including retinal amacrine and ganglion cells, Müller cells, retinal pigmented epithelium, and cells in the choroid, and likely has a broad range of visual and regulatory functions.

Immunocytochemical characterization of quisqualic acid- and N-methyl-D-aspartate-induced excitotoxicity in the retina of chicks.

A single, large dose of N-methyl-D-aspartate (NMDA) or quisqualic acid (QA) injected into the chick eye has been shown previously to destroy many retinal amacrine cells and to induce excessive ocular growth accompanied by myopia. The purpose of this study was to identify distinct populations of retinal cells, particularly those believed to be involved in regulating ocular growth, that are sensitive to NMDA or QA. Two pmol of NMDA or 0.2 micromol of QA were injected unilaterally into eyes of 7-day-old chicks, and retinas were prepared for observation 1, 3, or 7 days later. Retinal neurons were identified by using immunocytochemistry, and cells containing fragmented DNA were identified by 3'-nick-end labelling in frozen sections. NMDA and QA destroyed many amacrine cells, including those immunoreactive for vasoactive intestinal polypeptide, Met-enkephalin, and choline acetyltransferase, but they had little effect upon tyrosine hydroxylase-immunoreactive cells. Other cells affected by both QA and NMDA included those immunoreactive for glutamic acid decarboxylase, gamma-aminobutyric acid, parvalbumin, serotonin, and aminohydroxy methylisoxazole propionic acid (AMPA) receptor subunits GluR1 and GluR2/3. Cells largely unaffected by QA or NMDA included bipolar cells immunoreactive for protein kinase C (alpha and beta isoforms) and amacrine cells immunoreactive for glucagon. DNA fragmentation was detected maximally in many amacrine cells and in some bipolar cells 1 day after exposure to QA or NMDA. We propose that excitotoxicity caused by QA and NMDA induces apoptosis in specific populations of amacrine cells and that these actions are responsible for the ocular growth-specific effects of QA and NMDA reported elsewhere.

Identification and localization of muscarinic acetylcholine receptors in the ocular tissues of the chick.

The purpose of this study was to characterize the distribution of muscarinic acetylcholine receptors (mAChRs) in the ocular tissues of hatched chicks. In the chick, different isoforms of these receptors have been detected in the brain, heart, and retina, and mAChRs in ocular tissues have been implicated in the pathogenesis of form-deprivation myopia. However, the precise anatomical distribution of mAChRs within the retina, retinal pigment epithelium, choroid, ciliary body, and ciliary ganglion remains unknown. We used affinity-purified, type-specific antibodies directed to three different chick mAChR subtypes (cm2, cm3, and cm4) to detect receptor immunoreactivity in sections and extracts of these ocular tissues. We found cm2, cm3, and cm4 in the retina, retinal pigment epithelium, choroid, and ciliary body. Within the retina, cm2 was expressed in numerous amacrine and ganglion cells; cm3 was expressed in many bipolar cells and small subsets of amacrine cells; and cm4 was found in most, if not all, amacrine and ganglion cells. Each mAChR was localized to distinct strata within the inner plexiform layer that cumulatively form three broad bands that closely match previously described localizations of subtype-nonspecific muscarinic ligand binding. Only cm3 was detected in the outer plexiform layer, and only cm4 was detected in the ciliary ganglion. We propose that each mAChR subtype has unique functions in each ocular tissue.

Light-modulated release of RFamide-like neuropeptides from nervus terminalis axon terminals in the retina of goldfish.

The nervus terminalis of teleosts, a cranial nerve anatomically associated with the olfactory system, projects to visual system targets including retina and optic tectum. It is known to contain gonadotropin-releasing hormone and RFamide-like peptides, but its function remains unknown. We have probed nervus terminalis function in goldfish by measuring peptide content in retina and tectum with a radioimmunoassay for A18Famide (neuropeptide AF; bovine morphine-modulating peptide). We found that retinal peptide content increased in the dark and decreased in the light, whereas tectal peptide content decreased in the dark and increased in the light. In addition, RFamide-like peptide content in the retina was transiently decreased by severing both olfactory tracts, increased in light-adapted eyes treated with a GABAergic agonist (isoguvacine), and decreased in dark-adapted eyes treated with GABAergic antagonists (bicuculline and picrotoxin). We also found that RFamide-like peptide release could be induced in dark-adapted isolated-superfused retinas by exposure to light or a high concentration (102.5 mM) of potassium ions. We interpret the increase and decrease in peptide content as reflecting a decrease and increase, respectively, in rate of peptide release. We propose that the release and accumulation of RFamide-like peptides in axon terminals of nervus terminalis processes in the retina are modulated primarily by neurons intrinsic to the retina and regulated by light. Peptide release appears to be inhibited tonically in the dark by GABA acting through GABAA receptors; light facilitates peptide release by disinhibition due to a reduction in GABA release. In addition, we propose that electrical signals originating outside the retina can override these intrinsic release-modulating influences.

Immunocytochemical characterization of cysts in the peripheral retina and pars plana of the adult primate.

PURPOSE: To better characterize the cellular constituents of cysts in the peripheral retina and pars plana of the adult monkey. METHODS: Frozen sections of the peripheral retinal margin and pars plana from monkeys (Macaca nemestrina) between 1 and 15 years of age were stained with toluidine blue or immunolabeled with a variety of glia- and neuron-specific antibodies. RESULTS: In animals 1 to 2 years of age, the nonpigmented inner layer of the pars plana is a pseudostratified columnar epithelium. In these young animals, the peripheral retina had distinct layers and did not contain cysts. In animals 6 years of age or older, there were numerous cysts in the pars plana and in the peripheral retina. In the peripheral retina, neurons were randomly distributed and did not have a laminar organization. Cells surrounding cysts were immunoreactive for different types of markers for retinal neurons. Some of the cells surrounding cysts in the pars plana were also unexpectedly immunoreactive for antigens normally expressed only in retinal neurons and glia. CONCLUSIONS: Cysts form in the peripheral retina and pars plana in adult monkeys. The peripheral retinal cysts disrupt the normal lamination of the cells, but all types of retinal neurons are still present in the cysts. In an unexpected finding, cysts in the pars plana also contained cells immunoreactive for a few of the markers of retinal cells, suggesting that neurogenesis may occur in the pars plana of the adult primate.

Characterization of the RFamide-like neuropeptides in the nervus terminalis of the goldfish (Carassius auratus).

FMRFamide-immunoreactivity has been demonstrated in the CNS of many vertebrate species. We sought to further characterize this immunoreactivity in nervus terminalis retinal efferents of the goldfish using an antiserum raised against a bovine morphine modulating peptide (A18Famide). This antiserum robustly labels nervus terminalis efferents to the retina, as well as a sub-population of retinal amacrine cells. Under immunocytochemical conditions the antiserum cross-reacted with neuropeptide Y-like as well as A18Famide-like peptides, but under conditions of radioimmunoassay it was highly specific for A18Famide-like peptides. High pressure liquid chromatography, gel permeation chromatography and radioimmunoassay showed that at least two different RFamide-like peptides, approximately the same size as the bovine RFamide-like peptides, are present in the goldfish nervus terminalis.

Cholinergic amacrine cells are not required for the progression and atropine-mediated suppression of form-deprivation myopia.

Muscarinic cholinergic pathways have been implicated in the visual control of ocular growth. However, the source(s) of acetylcholine and the tissue(s) which regulate ocular growth via muscarinic acetylcholine receptors (mAChRs) remain unknown. We sought to determine whether retinal sources of acetylcholine and mAChRs contribute to visually guided ocular growth in the chick. Cholinergic amacrine cells were ablated by intraocular injections of either ethylcholine mustard aziridinium ion (ECMA; a selective cholinotoxin) or quisqualic acid (QA; an excitotoxin that destroys many amacrine cells, including those that release acetylcholine). Disruption of cholinergic pathways was assessed immunocytochemically with antibodies to the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT) and three different isoforms of mAChR, and by biochemical assay for ChAT activity. ECMA (25 nmol) destroyed two of the four subtypes of cholinergic amacrine cells and attenuated retinal ChAT activity, but left retinal mAChR-immunoreactivity intact. QA (200 nmol) destroyed the majority of all four subtypes of cholinergic amacrine cells, and ablated most mAChR-immunoreactivity and ChAT activity in the retina. ECMA and QA had no apparent effect on mAChRs or cholinergic fibres in the choroid, only marginally reduced choroidal ChAT activity, and had little effect on ChAT activity in the anterior segment. Toxin-treated eyes remained emmetropic and responded to form-deprivation by growing excessively and becoming myopic. Furthermore, daily intravitreal injection of 40 microg atropine for 6 days into form-deprived toxin-treated eyes completely prevented ocular elongation and myopia. We conclude that neither cholinergic amacrine cells nor mAChRs in the retina are required for visual regulation of ocular growth, and that atropine may exert its growth-suppressing influence by acting upon extraretinal mAChRs, possibly in the choroid, retinal pigmented epithelium, or sclera.

Vestibular hyperreactivity and hyperventilation after whiplash injury.

Vestibular, oculomotor and respiratory tests were performed on 32 patients after whiplash injury caused by a rear-end car collision. Oculomotor functions were generally normal. The cervico-ocular reflex was usually absent or displayed the low gain typical of normal subjects. There was no nystagmic response to static neck torsion. The vestibulo-ocular reflex showed vestibular hyperreactivity (VH) in a significantly large number of cases (n = 17; 53%). The respiratory test results were also typical of the hyperventilation syndrome (HVS) in a significantly large number of cases (n = 12; 38%). The findings of VH and the HVS were not significantly correlated within the patient group. However, the combination of VH and the HVS occurred significantly more often (n = 7; 22%) than could be accounted for by combined false positivity. Most of the significant findings were due to high relative frequencies in the women: 11 out of the 17 women (65%) showed VH, 8 (47%) had the HVS and 5 (29%) showed a combination of VH and the HVS. The findings were not correlated with the patient's age or the time interval between the accident and the examination. VH might have been the result of plastic adaptation to limited head mobility secondary to neck pain. Behavioural and emotional distress might offer alternative explanations for both VH and the HVS.