Does prophylactic decompression of distal nerves following nerve repair improve functional recovery? A systematic review.

BACKGROUND: Peripheral nerve injuries are burdensome on healthcare systems, individuals and society as a whole. The current standard of treatment for neurotmesis is primary neurorrhaphy or nerve grafting. However, several patients do not recover their full function. There has been a suggestion that primary distal neurolysis at common entrapment sites maximises surgical outcomes; however, no guidelines exist on this practice. This scoping review aims to ascertain the existing evidence on prophylactic distal decompression of peripheral nerves following repair. METHODS: A literature search was performed using Ovid Medline, PubMed, Embase and Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews for studies published in the past 50 years. Studies were screened using a selection criteria and study quality was assessed using standardised tools. Furthermore, thematic content analysis was performed. RESULTS: Six studies were eligible for inclusion after screening; all studies were retrospective and at most level 3 evidence. No studies were designed specifically to assess the efficacy of distal neurolysis following proximal repair, thus no comparative data with control cohorts are available. All studies that recommended distal decompression of proximally repaired nerves based their conclusions on cases observed by the authors in practice or from theories on nerve regeneration. CONCLUSIONS: This systematic review suggests that the evidence on the role of immediate distal neurolysis in primary neurorrhaphy is inadequate. Recommendations are limited by the lack of large-scale and generalisable data. Further research is needed with definitive objective outcomes and patient-related outcome measures.

Psammomatous melanotic schwannoma - a rare neck lump.

This case report discusses a cervical psammomatous melanotic schwannoma - a rare form of peripheral nerve sheath tumour - which may be highly vascular and is often associated with the Carney complex. Significant intraneural bleeding, which was encountered intraoperatively, was controlled successfully with a gelatine-based thrombin haemostatic agent (Floseal®, Baxter International, Deerfield, IL, USA) without complication.

Quantifying regeneration in patients following peripheral nerve injury.

Healthy nerve function provides humans with the control of movement; sensation (such as pain, touch and temperature) and the quality of skin, hair and nails. Injury to this complex system creates a deficit in function, which is slow to recover, and rarely, if ever, returns to what patients consider to be normal. Despite promising results in pre-clinical animal experimentation effective translation is challenged by a current inability to quantify nerve regeneration in human subjects and relate this to measurable and responsible clinical outcomes. In animal models, muscle and nerve tissue samples can be harvested following experimental intervention. This allows direct quantification of muscle mass and quality and quantity of regeneration of axons; such an approach is not applicable in human medicine as it would ensure a significant functional deficit. Nevertheless a greater understanding of this process would allow the relationship that exists between neural and neuromuscular regeneration and functional outcome to be more clearly understood. This article presents a combined commentary of current practice from a specialist clinical unit and research team with regard to laboratory and clinical quantification of nerve regeneration. We highlight how electrophysiological diagnostic methods (which are used with significant recognised limitations in the assessment of clinical medicine) can potentially be used with more validity to interpret and assess the processes of neural regeneration in the clinical context, thus throwing light on the factors at play in translating lab advances into the clinic.

An assessment of fatigability following nerve transfer to reinnervate elbow flexor muscles.

AIMS: Improvements in the evaluation of outcomes following peripheral nerve injury are needed. Recent studies have identified muscle fatigue as an inevitable consequence of muscle reinnervation. This study aimed to quantify and characterize muscle fatigue within a standardized surgical model of muscle reinnervation. PATIENTS AND METHODS: This retrospective cohort study included 12 patients who underwent Oberlin nerve transfer in an attempt to restore flexion of the elbow following brachial plexus injury. There were ten men and two women with a mean age of 45.5 years (27 to 69). The mean follow-up was 58 months (28 to 100). Repeated and sustained isometric contractions of the elbow flexors were used to assess fatigability of reinnervated muscle. The strength of elbow flexion was measured using a static dynamometer (KgF) and surface electromyography (sEMG). Recordings were used to quantify and characterize fatigability of the reinnervated elbow flexor muscles compared with the uninjured contralateral side. RESULTS: The mean peak force of elbow flexion was 7.88 KgF (sd 3.80) compared with 20.65 KgF (sd 6.88) on the contralateral side (p < 0.001). Reinnervated elbow flexor muscles (biceps brachialis) showed sEMG evidence of fatigue earlier than normal controls with sustained (60-second) isometric contraction. Reinnervated elbow flexor muscles also showed a trend towards a faster twitch muscle fibre type. CONCLUSION: The assessment of motor outcomes must involve more than peak force alone. Reinnervated muscle shows a shift towards fast twitch fibres following reinnervation with an earlier onset of fatigue. Our findings suggest that fatigue is a clinically relevant characteristic of reinnervated muscle. Adoption of these metrics into clinical practice and the assessment of outcome could allow a more meaningful comparison to be made between differing forms of treatment and encourage advances in the management of motor recovery following nerve transfer. Cite this article: Bone Joint J 2019;101-B:867-871.

A quantitative assessment of the functional recovery of flexion of the elbow after nerve transfer in patients with a brachial plexus injury.

AIMS: Improvements in the evaluation of outcome after nerve transfers are required. The assessment of force using the Medical Research Council (MRC) grades (0 to 5) is not suitable for this purpose. A ceiling effect is encountered within MRC grade 4/5 rendering this tool insensitive. Our aim was to show how the strength of flexion of the elbow could be assessed in patients who have undergone a re-innervation procedure using a continuous measurement scale. METHODS: A total of 26 patients, 23 men and three women, with a mean age of 37.3 years (16 to 66), at the time of presentation, attended for review from a cohort of 52 patients who had undergone surgery to restore flexion of the elbow after a brachial plexus injury and were included in this retrospective study. The mean follow-up after nerve transfer was 56 months (28 to 101, standard deviation (sd) 20.79). The strength of flexion of the elbow was measured in a standard outpatient environment with a static dynamometer. RESULTS: In total, 21 patients (81%) gained MRC grade 4 strength of flexion of the elbow. The mean force of flexion was 7.2 kgf (3 to 15.5, sd 3.3). CONCLUSION: This study establishes that the dynamometer may be used for assessing the strength of flexion of the elbow in the outpatient department after nerve reconstructive surgery. Cite this article: Bone Joint J 2016;98-B:1517-20.

Mycolactone-mediated neurite degeneration and functional effects in cultured human and rat DRG neurons: Mechanisms underlying hypoalgesia in Buruli ulcer.

BACKGROUND: Mycolactone is a polyketide toxin secreted by the mycobacterium Mycobacterium ulcerans, responsible for the extensive hypoalgesic skin lesions characteristic of patients with Buruli ulcer. A recent pre-clinical study proposed that mycolactone may produce analgesia via activation of the angiotensin II type 2 receptor (AT2R). In contrast, AT2R antagonist EMA401 has shown analgesic efficacy in animal models and clinical trials for neuropathic pain. We therefore investigated the morphological and functional effects of mycolactone in cultured human and rat dorsal root ganglia (DRG) neurons and the role of AT2R using EMA401. Primary sensory neurons were prepared from avulsed cervical human DRG and rat DRG; 24 h after plating, neurons were incubated for 24 to 96 h with synthetic mycolactone A/B, followed by immunostaining with antibodies to PGP9.5, Gap43, ß tubulin, or Mitotracker dye staining. Acute functional effects were examined by measuring capsaicin responses with calcium imaging in DRG neuronal cultures treated with mycolactone. RESULTS: Morphological effects: Mycolactone-treated cultures showed dramatically reduced numbers of surviving neurons and non-neuronal cells, reduced Gap43 and ß tubulin expression, degenerating neurites and reduced cell body diameter, compared with controls. Dose-related reduction of neurite length was observed in mycolactone-treated cultures. Mitochondria were distributed throughout the length of neurites and soma of control neurons, but clustered in the neurites and soma of mycolactone-treated neurons. Functional effects: Mycolactone-treated human and rat DRG neurons showed dose-related inhibition of capsaicin responses, which were reversed by calcineurin inhibitor cyclosporine and phosphodiesterase inhibitor 3-isobutyl-1-Methylxanthine, indicating involvement of cAMP/ATP reduction. The morphological and functional effects of mycolactone were not altered by Angiotensin II or AT2R antagonist EMA401. CONCLUSION: Mycolactone induces toxic effects in DRG neurons, leading to impaired nociceptor function, neurite degeneration, and cell death, resembling the cutaneous hypoalgesia and nerve damage in individuals with M. Ulcerans infection.

Nerve injuries associated with supracondylar fractures of the humerus in children: our experience in a specialist peripheral nerve injury unit.

AIMS: We aimed to identify the pattern of nerve injury associated with paediatric supracondylar fractures of the humerus. PATIENTS AND METHODS: Over a 17 year period, between 1996 and 2012, 166 children were referred to our specialist peripheral nerve injury unit. From examination of the medical records and radiographs were recorded the nature of the fracture, associated vascular and neurological injury, treatment provided and clinical course. RESULTS: Of the 166 patients (111 male, 55 female; mean age at time of injury was seven years (standard deviation 2.2)), 26 (15.7%) had neurological dysfunction in two or more nerves. The injury pattern in the 196 affected nerves showed that the most commonly affected nerve was the ulnar nerve (43.4%), followed by the median (36.7%) and radial (19.9%) nerves. A non-degenerative injury was seen in 27.5%, whilst 67.9% were degenerative in nature. Surgical exploration of the nerves was undertaken in 94 (56.6%) children. The mean follow-up time was 12.8 months and 156 (94%) patients had an excellent or good clinical outcome according to the grading of Birch, Bonney and Parry. CONCLUSION: Following paediatric supracondylar fractures we recommend prompt referral to a specialist unit in the presence of complete nerve palsy, a positive Tinel's sign, neuropathic pain or vascular compromise, for consideration of nerve exploration. TAKE HOME MESSAGE: When managed appropriately, nerve recovery and clinical outcomes for this paediatric population are extremely favourable. Cite this article: Bone Joint J 2016;98-B:851-6.

Pediatric fractures and dislocations of the hip and pelvis.

Recognition of an unstable pelvic fracture or a significant hip injury in children is important. Clinical assessment plays a valuable role as does the judicious use of imaging modalities in determining the most effective form of treatment, but the routine use of the standard AP pelvic radiograph is questioned. The concept of age and skeletal maturity has been re-evaluated, allowing the appropriate identification of cases that would benefit from an aggressive operative approach. A dual-tier approach to the treatment of pediatric pelvic trauma is suggested with an appreciation that there is no substantial evidence base for the surgical treatment of most injuries. Displaced femoral neck fractures and injuries to the hip joint that damage the articular or physeal cartilages require careful assessment and prompt and careful reduction and stabilization.

Differences in the Composition of Adhesive and Non-Adhesive Mucus From the Limpet Lottia limatula.

The mucus used by the limpet Lottia limatula to form glue-like attachments was compared biochemically to the slippery mucus produced during other activities, such as suction adhesion. Colorimetric assays revealed the protein content of the adhesive mucus to be 2.1 times greater than that of the non-adhesive form, and the carbohydrate content to be 1.9 times greater. Both forms of mucus contained roughly six times as much protein as carbohydrate, and there was no difference in their inorganic elemental compositions. Quantitative analysis of the protein content by SDS-PAGE and a scanning densitometer revealed a similar protein composition in both forms of mucus; but three notable differences emerged. First, the overall difference in protein concentration was confirmed. In addition, there was a 118 kD protein that was common only in the adhesive mucus, and a 68 kD protein that occurred only in the non-adhesive mucus.

Control of retinoic acid receptor expression in mouse melanoma cells by cyclic AMP.

Retinoic acid receptor (RAR) alpha and gamma mRNAs were constitutively expressed in B16 melanoma cells with or without retinoic acid (RA) treatment. RAR beta mRNA, however, was significantly expressed only after exposure to RA. Induction of RAR beta by RA occurred within 1 h and was not inhibited by cycloheximide (i.e., did not require new protein synthesis). All three RAR mRNA levels were dramatically decreased with 8-bromo-cyclic AMP treatment and could not be rescued by addition of RA. Analysis of RAR gamma revealed that this decrease occurred within 1 h of exposure to 8-bromo-cyclic AMP and was not blocked by simultaneous treatment with cycloheximide. The stability of RAR gamma mRNA was not altered by cyclic AMP treatment. Nuclear extracts from 8-bromo-cyclic AMP-treated cells showed a large decrease in protein binding to a retinoic acid response element (RARE) oligonucleotide compared to control cells. This correlated with a marked reduction of RA-stimulated RARE-reporter gene activity in transfected cells which were treated with cyclic AMP. Pretreatment of B16 cells with cyclic AMP prior to RA addition dramatically reduced induction of PKC alpha, an early marker of RA-induced cell differentiation. Thus, cyclic AMP can antagonize the action of RA most likely via its ability to inhibit RAR expression.

N-(4-hydroxyphenyl)retinamide (4-HPR)-mediated biological actions involve retinoid receptor-independent pathways in human breast carcinoma.

Retinoid response pathways involve retinoic acid receptors (RARs) and retinoid X receptors. N-(4-hydroxyphenyl) retinamide (4-HPR), a derivative of all-trans-retinoic acid (RA) is currently in clinical trials as a chemopreventive agent for breast cancer. The issue whether 4-HPR mediates its biological actions via classical retinoid receptor pathways remains to be investigated. In this study, we provide several lines of evidence that 4-HPR mediates its biological actions via a novel pathway(s) that does not involve the classical retinoid receptor pathways. For example, 4-HPR was more potent than RA as an antiproliferative agent and inhibited growth of otherwise RA-resistant human breast carcinoma cells. Exposure to 4-HPR resulted in the generation of DNA fragmentation with subsequent cell death in both RA-positive estrogen receptor (ER)-positive as well as RA-refractory ER-negative breast carcinoma cell lines. N-(4-Methoxyphenyl)retinamide (4-MPR), which is the major 4-HPR metabolite in circulation, was biologically inert in this system. 4-HPR and 4-MPR bound poorly to the RAR alpha, beta and gamma in vitro and only minimally activated the retinoic acid receptor element (RARE) and retinoid X receptor response elements (RXREs) in human breast carcinoma cells. Neither 4-HPR nor 4-MPR are metabolized to any of the known conventional retinoids. In addition, 4-HPR or 4-MPR transactivation of RAREs or RXREs transfected into MCF-7 and MDA-MB-231 cells was not noted at 48 h. Nevertheless 4-HPR-mediated cell death was observed at 48 h, further suggesting that neither 4-HPR nor 4-MPR are metabolized to retinoids which activate the RAREs or RXREs in breast carcinoma cells. Furthermore, unlike RA, which exhibited anti-AP1 activity, 4-HPR inhibition of growth did not involve anti-AP1 activity. These results suggest that 4-HPR acts by a unique pathway that is not mediated by retinoid receptors.

Correlation of retinoid binding affinity to retinoic acid receptor alpha with retinoid inhibition of growth of estrogen receptor-positive MCF-7 mammary carcinoma cells.

Both anchorage-dependent growth and anchorage-independent growth of the estrogen receptor-positive mammary carcinoma cell line MCF-7 are inhibited by all-trans-retinoic acid. This cell line has nuclear retinoic acid receptors (RARs) alpha and gamma. The natural retinoids all-trans-retinoic acid and 9-cis-retinoic acid and a series of 12 conformationally restricted retinoids, which showed a range of binding selectivities for these receptors and had either agonist or antagonist activity for gene transcriptional activation by the RARs, were evaluated for their abilities to inhibit anchorage-dependent (adherent) and anchorage-independent (clonal) growth of MCF-7 cells. Correlation analyses were performed to relate growth inhibition by these retinoids with their binding affinity to RAR alpha or RAR gamma. Inhibition of anchorage-dependent growth in culture after 7 days of retinoid treatment correlated with binding to RAR alpha (n = 14; P < or = 0.001) and not to RAR gamma (n = 14; P > 0.1). Both the RAR alpha-selective retinoid agonists and the two RAR antagonists that were evaluated inhibited adherent cell growth. The RAR gamma-selective agonists had very low growth inhibitory activity (< 10%) at concentrations as high as 12.5 microM. These results suggest that RAR alpha is the retinoid receptor involved in the inhibition of adherent cell growth by retinoids and that transcriptional activation by this receptor on a RAR response element does not appear to be required for this process to occur. For this series of retinoids, inhibition of anchorage-independent growth after 21 days of retinoid treatment only correlated (n = 12; P < or = 0.005) with binding affinity to RAR alpha for the retinoid agonists, although the RAR gamma-selective retinoids displayed weak activity. The RAR antagonists were very poor inhibitors of growth. These results suggest that activation of gene transcription by RAR alpha appears to be required for inhibition of anchorage-independent growth by retinoids in this estrogen receptor-positive mammary carcinoma cell line.

Identification of structurally altered estrogen receptors in human breast cancer by site-directed monoclonal antibodies.

We have developed and characterized site-directed monoclonal (MAb) and polyclonal antibodies to a specific domain in the N-terminal A/B region in order to assess estrogen receptor (ER) structural integrity in human breast tumor samples. The antibodies (Abs) reacted specifically with the native (undenatured) ER from various species. The synthetic peptides competed effectively for ER binding to the Abs, suggesting site-specificity. The Abs recognized the activated (4S) and transformed (5S) but not the unactivated, untransformed, molybdate-stabilized (8S) ER, suggesting that the epitope is inaccessible in the 8S form. Some of these Abs reacted with ER bound to its responsive elements, as determined by gel mobility shift assay. To evaluate the structural integrity of ER in breast cancer, we have utilized a) ligand binding analysis for the hormone binding domain; b) site-directed MAb to the DNA-binding domain; and c) site-directed MAb to the N-terminal transactivation domain. Analysis of ER from 29 human breast tumors revealed that 10 out of 29 tumors (35%) contained ER with intact hormone-, DNA-, and N-terminal domains. Thirteen out of 29 tumors (approximately 45%) contained ER with intact hormone binding and N-terminal domains but were defective only in the DNA-binding domain. Three out of 29 tumors (approximately 10%) contained ER defective only in the N-terminal domain. Another subgroup of tumors (3/29; approximately 10%) had ER with normal hormone binding domain but were defective in both the DNA-binding and the N-terminal activation domains.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of human retinoic acid receptor alpha 1 expressed in recombinant baculovirus-infected Sf9 insect cells.

Full-length human retinoic acid receptor alpha 1 (hRAR alpha 1) was expressed in Sf9 insect cells using the baculovirus expression vector system (BEVS). Western blot analysis using a specific anti-RAR peptide antiserum detected two major protein bands with apparent mol wts of approximately 54 and approximately 51 kDa in extracts from insect cells infected with recombinant hRAR alpha 1 Autographica californica (AcNPV) baculovirus. Analysis of recombinant extracts from Sf9 cells labeled in vivo with [32P]orthophosphate suggested that the recombinant protein was phosphorylated. A component in the recombinant nuclear extracts specifically bound [3H]all-trans-retinoic acid (RA) and sedimented in sucrose density gradient centrifugation as a single, symmetric peak with a sedimentation coefficient of approximately 3.6S, corresponding to a protein of approx 50 kDa. Scatchard analyses determined that [3H]RA was bound in recombinant extracts by a single class of binding sites with an apparent dissociation constant of approximately 0.3 nM and nuclear and cytoplasmic extracts contained approximately 1200 and approximately 200 pmoles, respectively, of unoccupied receptor per mg protein. In competitive ligand binding assays, relative binding affinities of 9-cis- and 13-cis-RA for hRAR alpha 1 in nuclear extracts were about threefold and sixfold lower than all-trans-RA, whereas all-trans-retinol, -retinaldehyde, and -retinyl acetate demonstrated relatively weak binding. In gel mobility shift assays, the electrophoretic migration of a [32P]-labeled oligonucleotide containing the retinoic acid response element of the RAR beta gene was retarded in the presence of recombinant nuclear and cytoplasmic extracts. The apparent complex formation between recombinant hRAR alpha 1 and beta RARE was greatly enhanced by the addition of nuclear extract from wild-type AcNPV-infected Sf9 cells, possibly because of heterodimer formation between recombinant hRAR alpha 1 and a metazoan RXR homolog. Thus, recombinant hRAR alpha 1 expressed at high levels in Sf9 insect cells exhibited biochemical properties of the native protein, including nuclear translocation, specific high affinity ligand and RARE binding, and possible heterodimer formation.

Intestinal vitamin A metabolism: coordinate distribution of enzymes and CRBP(II).

In the mucosal layer of the small intestine, we found nearly identical gradients of CRBP(II), retinal reductase, and LRAT levels down the duodenal-ileal axis, suggesting coordinate regulation of these three proteins. In all cases the level of binding protein or enzyme activity was greatest in the proximal intestine and then decreased sharply in the distal half. This pattern fits with the known capacity of the intestine to absorb vitamin A. In addition, the retinal reductase activity was found predominantly in the intestinal mucosa, while LRAT activity was found in both the intestinal mucosa and muscle. An even distribution of LRAT activity along the longitudinal axis of the intestinal muscle was consistent with an even distribution of CRBP in that tissue. In conjunction with LRAT activity and CRBP, we found endogenous retinyl ester stores in the intestinal muscle layer. The patterns of retinyl ester produced by LRAT in vitro and found in vivo were similar, with retinyl palmitate predominating and a high percentage comprised of retinyl stearate. We also observed a bile salt-independent retinyl ester hydrolase activity in intestinal muscle whose distribution paralleled the retinyl ester stores and LRAT levels. This hydrolase appears to be distinct from retinyl ester hydrolases described from other organs as its activity was insensitive to retinyl ester chain length, the presence of bile salts, or the addition of apo-CRBP. This activity was inhibited by diethyl-p-nitrophenyl-phosphate (IC50 100 microM) and diethylpyrocarbonate (IC50 10 microM), demonstrating a requirement for active serine and histidine residues. In addition, we describe an activity present in some intestinal microsomal preparations that can perturb determinations of reductase and LRAT activity and must be avoided.

Ontogeny of two vitamin A-metabolizing enzymes and two retinol-binding proteins present in the small intestine of the rat.

The patterns of expression of cellular retinol-binding protein (CRBP), cellular retinol-binding protein, type two [CRBP(II)], lecithin: retinol acyltransferase (LRAT), and microsomal retinal reductase were examined for rat small intestine during the perinatal period. CRBP was present (15 pmole per mg soluble protein) at the earliest time examined, the 16th day of gestation, declining by 70% by birth, maintained to adulthood. In contrast, CRBP(II) appeared 2-3 days before birth, rising to its highest level (500 pmole per mg soluble protein) by day 3 after birth, then declining by 50% during the late suckling period to the adult level. Immunohistochemistry revealed that CRBP(II) initially appeared in the epithelial cell layer in a patchy manner, resolving by birth into an even staining of all villus-associated enterocytes. In contrast, CRBP was evenly expressed in the epithelial cell layer at day 17/18 but was absent by birth. Intestinal LRAT activity increased rapidly in the 2 days prior to birth, then declined at weaning to the adult level. Microsomal retinal reductase was measurable in the intestine at birth, but not detected during the early suckling period, reappearing at day 21. Considerable increase was then observed coincident with weaning, when carotenes, from which retinal is derived, became an important source of vitamin A. The pattern of appearance of these elements appears to prepare the intestine for the necessary processing of vitamin A required after birth.

Residual toxicity of four insecticides to Aedes triseriatus in scrap tires.

Four insecticides were tested for residual activity to Aedes triseriatus in scrap tires. Abate (temephos) granules applied at 10 ppm (AI) resulted in 100% mortality of 4th instar larvae for more than one year. The other insecticides caused no mortality within 4 wk after application.

Vitamin A metabolism in the human intestinal Caco-2 cell line.

The human intestinal Caco-2 cell line, described as enterocyte-like in a number of studies, was examined for its ability to carry out the metabolism of vitamin A normally required in the absorptive process. Caco-2 cells contained cellular retinol-binding protein II, a protein which is abundant in human villus-associated enterocytes and may play an important role in the absorption of vitamin A. Microsomal preparations from Caco-2 cells contained retinal reductase, acyl-CoA-retinol acyltransferase (ARAT), and lecithin-retinol acyltransferase (LRAT) activities, which have previously been proposed to be involved in the metabolism of dietary vitamin A in the enterocyte. When intact Caco-2 cells were provided with beta-carotene, retinyl acetate, or retinol, synthesis of retinyl palmitoleate, oleate, palmitate, and small amounts of stearate resulted. However, exogenous retinyl palmitate or stearate was not used by Caco-2 cells as a source of retinol for ester synthesis. While there was a disproportionate synthesis of monoenoic fatty acid esters of retinol in Caco-2 cells compared to the retinyl esters typically found in human chylomicrons or the esters normally synthesized in rat intestine, the pattern was consistent with the substantial amount of unsaturated fatty acids, particularly 18:1 and 16:1, found in the sn-1 position of Caco-2 microsomal phosphatidylcholine, the fatty acyl donor for LRAT. Both ARAT and LRAT have been proposed to be responsible for retinyl ester synthesis in the enterocyte.(ABSTRACT TRUNCATED AT 250 WORDS)