Anatomy of the superior hypogastric plexus and its application in nerve-sparing paraaortic lymphadenectomy.

BACKGROUND: The purpose of this study was to clarify the anatomy of the superior hypogastric plexus, which would contribute to advancement of nerve-sparing paraaortic lymphadenectomy. MATERIALS AND METHODS: Eighteen cadavers were dissected and morphometrically analysed based on photographic images. Anatomical landmarks such as aortic bifurcation, transitional points of abdominal aorta to bilateral common iliac arteries, and cross point of the right ureter and pelvic brim, and cross point of sigmoid mesentery and pelvic brim were selected as reference points. RESULTS: The left lowest lumbar splanchnic nerve was located more laterally to transitional point of abdominal aorta to in 11/18 specimens, whereas the right lowest lumbar splanchnic nerve passed onto the right transitional point in only one specimen. The lowest lumbar splanchnic nerves or the superior hypogastric plexus covered the aortic bifurcation in 11/18 specimens. The superior hypogastric plexus was separate from the cross point of right ureter and pelvic brim as well as cross point of sigmoid mesentery and pelvic brim. CONCLUSIONS: The superior hypogastric plexus is at risk of injury during paraaortic lymphadenectomy because of its topography. Preservation of the superior hypogastric plexus regarding its anatomic basis during paraaortic lymphadenectomy is required.

Providing essential clinical care for non-COVID-19 patients in a Seoul metropolitan acute care hospital amidst ongoing treatment of COVID-19 patients.

We assessed infection control efforts by comparing data collected over 20 weeks during a pandemic under a dual-track healthcare system. A decline in non-COVID-19 patients visiting the emergency department by 37.6% (P<0.01) was observed since admitting COVID-19 cases. However, patients with acute myocardial infarction (AMI), stroke, severe trauma and acute appendicitis presenting for emergency care did not decrease. Door-to-balloon time (34.3 (± 11.3) min vs 22.7 (± 8.3) min) for AMI improved significantly (P<0.01) while door-to-needle time (55.7 (± 23.9) min vs 54.0 (± 18.0) min) in stroke management remained steady (P=0.80). Simultaneously, time-sensitive care involving other clinical services, including patients requiring chemotherapy, radiation therapy and haemodialysis did not change.

Zuckerkandl Tubercle of the Thyroid Gland: Correlations between Findings of Anatomic Dissections and CT Imaging.

BACKGROUND AND PURPOSE: The Zuckerkandl tubercle is located at the posteromedial border of the thyroid lobe, and it may be confused with a neoplasm or other mass. This study was performed to clarify the position and morphologic characteristics of the Zuckerkandl tubercle by dissecting cadavers and to compare the findings with the corresponding CT images obtained in the same cadavers. MATERIALS AND METHODS: One hundred thyroid lobes from 50 fresh cadavers were dissected for this study (20 males and 30 females; mean age at death, 77.3 ± 11.5 years). CT scans were obtained in 10 of the cadavers by using a 128-channel multidetector row CT scanner before dissection. RESULTS: The Zuckerkandl tubercle of the thyroid gland was observed in 83% of the specimens. It was mostly located at the posteromedial border of the thyroid lobe and within the middle two quarters (2nd and 3rd) of the thyroid lobe. The Zuckerkandl tubercle was classified into 3 types based on its direction of extension: posteromedial in 64% of the specimens, posteromedial and superior in 13%, and posteromedial and inferior in 6%. On axial CT, the Zuckerkandl tubercle was usually continuous with the posteromedial part of the thyroid lobe and extended posteromedially to the esophagus. The parts of the Zuckerkandl tubercle that protrude posteromedially and superiorly or posteromedially and inferiorly from the thyroid lobe appeared separated from the thyroid gland by a thin, low-density string on axial CT. CONCLUSIONS: Zuckerkandl tubercles that protrude toward the posteromedial and superior or inferior direction could cause confusion due to their separation when performing diagnoses with CT images.

Separate muscle bundles of the flexor digitorum superficialis overlying the ulnar nerve.

BACKGROUND: The aim of this study was to elucidate the morphological charac-teristics of the muscle bundles of the flexor digitorum superficialis (FDS) attached to the intermuscular aponeurosis (IMA) and any related structure that could potentially compress the ulnar nerve. MATERIALS AND METHODS: Fifty embalmed limbs of 34 adult cadavers were studied. RESULTS: The FDS arose as multiple separate bundles from the IMA of the lateral surface of the flexor carpi ulnaris in 76% of specimens. Below their origin, these separate bundles became attached continuously as a single mass to form the muscle belly. There were 1, 2, 3, 4 and 5 arising FDS muscle bundles in 28%, 30%, 4%, 10% and 4% of specimens, respectively. The muscle bundles were attached either only superficially (24% of cases) or across the entire width (20% of cases) of the IMA. In 32% of the specimens, bundles arose from the IMA in a combined fashion, being attached to the IMA superficially, deep and across the entire structure. The muscle bundles that arose from the deep part or entire width of the IMA were in contact with the ulnar nerve in 52% of specimens. In 11 (22%) specimens, the deep borders of the lowest muscle bundles close to the ulnar nerve were composed of tendinous fibres that divided from the IMA of the lateral surface of the flexor carpi ulnaris. The distance from the medial epicondyle to the lowest point of the FDS arising from the IMA was 62.0 ± 19.7 mm. CONCLUSIONS: The thick tendinous deep border of the lowest muscle bundle of the FDS where it attaches to the IMA is a potential cause of ulnar nerve compression.

The nutritional value of degermed, dehulled corn for pigs and its impact on the gastrointestinal tract and nutrient excretion.

Three experiments were designed to assess the feeding value and potential environmental benefits of feeding degermed, dehulled corn, a low fiber by-product originating from the corn dry milling process, to pigs. Twelve 27-kg (SE = 0.8) barrows were used in Exp. 1 to measure the apparent fecal digestibility of DM, GE and N of degermed, dehulled corn compared with corn grain. Two diets were formulated to contain either 96.4% of degermed, dehulled corn or corn grain plus supplemental vitamins and minerals. Digestibilities of DM, GE, and N were greater in degermed, dehulled corn (96.2, 96.0, and 93.6%, respectively) compared with corn grain (89.0, 89.0, and 78.4%, respectively) (P < 0.01). Overall, a 67 and 29% reduction in DM and N excretion, respectively, was observed. In Exp. 2, eight 70-kg (SE =1.8) barrows were surgically fitted with ileal cannulae and fed the same diets as in Exp. 1, to measure the ileal digestibility of nutrients in degermed, dehulled corn. Ileal digestibility of DM, energy, and N was 13, 15, and 7% greater in degermed, dehulled corn (P < 0.05). Apparent ileal digestibility coefficients of leucine, methionine, and phenylalanine were greater in degermed, dehulled corn compared with corn grain (P < 0.05) while a trend for a lower tryptophan digestibility in degermed, dehulled corn was observed (P = 0.067). In Experiment 3, 96 nursery pigs with an initial average BW of 8.8 kg (SE = 0.08), fed a starter diet formulated with degermed, dehulled corn or corn grain as the major grain source, were used in a 28-d growth performance study. At the end of the study, 24 pigs (1 pig per pen) were sacrificed and gastrointestinal tract measurements were taken. Daily growth rates of pigs were the same between diets (0.64 kg/d). A trend for reduced feed intake (P = 0.073) in pigs fed degermed, dehulled corn led to a 4% improvement in gain to feed (P < 0.05). Feeding degermed, dehulled corn had no effect on gut fill, gastrointestinal tract weight, or liver weight (P > 0.05). Ileal villus lengths and crypt depths were not affected by feeding degermed, dehulled corn although ileal villus widths were greater in pigs fed corn grain. Results from these trials suggest that corn processed to remove poorly digestible fiber fractions provides more digestible nutrients than corn grain. As a result, degermed, dehulled corn reduces fecal and N excretion, thus providing a means to reduce nutrient excretion.

Regional and processor variation in the ileal digestible amino acid content of soybean meals measured in growing swine.

To assess differences in soybean meal quality related to region of production, researchers in Illinois, Kansas, North Carolina, The Netherlands, and Ohio collected four soybean meal samples processed locally at least 15 d apart. These samples were assayed for ileal amino acid digestibility by pigs using a common soybean meal and a soy protein concentrate as references, and a low-protein casein diet for determination of endogenous amino acid losses. Digestibility was determined at each university using seven barrows surgically fitted with ileal cannulas in a 7 x 7 Latin square design. The experimental diets contained 17% CP from the test material except for the low-protein casein diet. Animals were fed twice daily, 12 h apart, at a level of 45 g x kg(-0.75) BW for each meal. Following a 5-d adaptation period, ileal digesta were collected for two 12-h periods for 2 d to be used for determination of ileal digestibility. Variation in amino acid digestibility was very small among and within sites and was much smaller than variation in the concentration of amino acids. Among sites, samples from The Netherlands had less total and thus digestible lysine and methionine than the U.S. samples (P < 0.05). The soybean meals tested in this experiment were approximately 4% higher in amino acids than that reported in the NRC (1998). True (standardized) digestibilities, however, were very similar to NRC values except for cysteine and threonine, which were 5 and 3 percentage points lower in this experiment, respectively. In conclusion, soybeans grown in the United States and locally processed into soybean meal were very similar in nutritional composition. Soybean meals produced in The Netherlands were lower in lysine and methionine (P < 0.05) but had a digestibility similar to that produced in the United States.

Light- and electron-microscopic analysis of neuropeptide Y-immunoreactive amacrine cells in the guinea pig retina.

We investigated the morphology and synaptic connections of neuropeptide Y (NPY)-containing neurons in the guinea pig retina by immunocytochemistry, using antisera against NPY. Specific NPY immunoreactivity was localized to a population of wide-field and regularly spaced amacrine cells with processes ramifying mainly in stratum 1 of the inner plexiform layer (IPL). Double-label immunohistochemistry demonstrated that all NPY-immunoreactive cells possessed glutamic acid decarboxylase 65 immunoreactivity. The synaptic connectivity of NPY-immunoreactive amacrine cells was identified in the IPL by electron microscopy. The NPY-labeled amacrine cell processes received synaptic input from other amacrine cell processes and bipolar cell axon terminals in stratum 1 of the IPL. The most frequent postsynaptic targets of NPY-immunoreactive amacrine cells were other amacrine cell processes. Synaptic outputs to bipolar cells were also observed in a small number of cases. This finding suggests that NPY-containing amacrine cells may influence inner retinal circuitry in stratum 1 of the IPL, thus mediating visual processing.

Reorganization of horizontal cell processes in the developing FVB/N mouse retina.

We investigated the morphological changes of horizontal cells after postnatal photoreceptor degeneration in the developing FVB/N mouse retina, using immunocytochemistry with anti-calbindin D-28K. From postnatal day 14 (P14) onwards, processes emerging from horizontal cells descend into the inner plexiform layer (IPL) and ramify mainly in stratum 1 of the IPL. Electron microscopy revealed that the descending processes make synaptic contacts with bipolar cells in the outer plexiform layer. Our results clearly demonstrate that loss of photoreceptor cells induces the reorganization of horizontal cell processes in the retinas of FVB/N mice as they mature.

The regulatory expression of neuronal nitric oxide synthase in the ischemic rat retina.

We investigated the expression and cellular localization of neuronal nitric oxide synthase (nNOS) in the rat retina, following ischemic injury induced by transient increase of intraocular pressure. In the normal retina, nNOS immunoreactivity was localized to certain populations of amacrine cells, displaced amacrine cells and a few bipolar cells. Following transient ischemia, retinal neurons expressing the immunoreactivity increased and peaked three days after reperfusion. Quantitative evaluation using immunoblotting confirmed that nNOS expression showed a peak value (500% of control levels) at 3 days, and then decreased again to 150% of controls by 4 weeks after reperfusion. Our findings suggest that this over-produced NO may act as a neurotoxic agent in the ischemic rat retina.

Morphological analysis of CD15-immunoreactive neurons in the guinea pig retina.

Using immunocytochemistry, morphometry and electron microscopy, we have investigated the distribution and characteristics of CD15-immunoreactive (IR) neurons in the guinea pig retina. In the present study, two types of amacrine cells, including interplexiform cells in the inner nuclear layer (INL) and some cells in the ganglion cell layer (GCL), were labeled with anti-CD15 antisera. Type 1 amacrine cells had large somata located in the INL, with long and branched processes ramifying mainly in strata 4 and 5 of the inner plexiform layer (IPL). Somata of type 2 cells had smaller diameters, and were also located in the INL. Their processes stratified in stratum 1. The densities of type I and type 2 amacrine cells increased from 152.8+/-36.7/mm2 and 160.6+/-61.7/mm2 in the peripheral retina, to 404.3+/-41.5/mm2 and 552.2+/-72.2/mm2 in the central retina, respectively. Cells in the GCL exhibiting CD15 immunoreactivity were rarely observed. Colocalization experiments, using consecutive semi-thin sections, demonstrated that these CD15-IR amacrine cells exhibited gamma-aminobutyric acid (GABA) immunoreactivity. In addition, the processes of the type 1 cells formed one member of the postsynaptic dyads that are formed in the axon terminals of rod bipolar cells. Most of these processes made reciprocal synapses back to the axon terminals of the rod bipolar cells. Thus, CD15-IR amacrine cells constitute a subpopulation of GABAergic amacrine cells in the guinea pig retina, and the type 1 cells among them provide the inhibitory input to rod bipolar cells.

Choline acetyltransferase-immunoreactive neurons in the developing rat retina.

The development of cholinergic cells in the rat retina has been examined with immunocytochemistry by using antisera against choline acetyltransferase (ChAT). ChAT-immunoreactive (IR) cells were first detected at embryonic day 17 (E17) in the transitional zone between the neuroblastic layer (NBL) and ganglion cell layer (GCL). At E20, ChAT-IR cells are located exclusively in the GCL. At postnatal day 0 (P0), ChAT immunoreactivity appeared for the first time in cells at the distal margin of the NBL. Two prominent bands of labeled processes were first visible at P3, and by P15, these two bands resembled those of the adult retina. In addition, ChAT immunoreactivity appeared transiently in horizontal cells from P5 to P10. The number of ChAT-IR cells increased steadily up to P15. This resulted in a 93.8-fold increase between E17 and P15 (680-63,800 cells). However, after P15, the number declined by 19% from 63,800 cells at P15 to 51,800 in the adult. At all ages, the spatial density of each ChAT-IR cell population in the central retina was higher than in the periphery. In both central and peripheral regions, the peak density of ChAT-IR cells in the GCL was attained at E20. However, in the INL, the peak densities occurred at P3 in the central region and at P5 in the peripheral region. Up to P15, the soma diameter of ChAT-IR cells in the INL and GCL in each region increased continuously, reaching peak values at P15. Our results demonstrate that ChAT immunoreactivity is expressed in early developmental stages in the rat retina, as in other mammals, and that acetylcholine released from ChAT-IR cells may have neurotrophic functions in retinal maturation.

Neuronal nitric oxide synthase immunoreactive neurons in the mammalian retina.

The development of immunocytochemistry has led to a better understanding of synaptic transmission carried out by neuroactive substances in the mammalian brain, including the retina. In the mammalian retina, nitric oxide (NO) is widely accepted as a neuromodulator. Histochemistry based on NADPH-d and immunocytochemistry based on nitric oxide synthase (NOS) have been used to identify the presence of nitric oxide in the mammalian retina. Certain types of amacrine cells and a class of displaced amacrine cells have been labeled consistently in all mammalian retinae studied to date. Other cell types showing NADPH-d reactivity or NOS immunoreactivity varied between species. NADPH-d reactive or NOS immunoreactive amacrine cells may serve as a source of NO for amacrine, bipolar, and ganglion cells in the inner retina, whereas interplexiform cells, bipolar cells, and horizontal cells may serve as a source of NO for the outer retina of mammals.

Selective neuronal survival and upregulation of PCNA in the rat inner retina following transient ischemia.

In this study we investigated the extent and time course of neuronal cell death and the regulation of the proliferating cell nuclear antigen (PCNA) in the different retinal cell layers following ischemia-reperfusion injury. Retinal ischemia was induced by controlled elevation of the intraocular pressure for a duration of 60 min. Changes in thickness and cell numbers in the retinal cell layers were analyzed at various time points (1 h to 4 weeks) after reperfusion. In parallel, apoptotic cell death was determined by the TUNEL method and the expression of PCNA analyzed by immunocytochemistry. In addition, we tested whether PCNA is expressed in neurons by double immunocytochemistry. The reduction in thickness was found to be less pronounced in the inner nuclear layer (INL). Correspondingly, cell numbers decreased by only 33% in the inner retina, but by more than 80% in the outer nuclear layer (ONL). Alterations in glial cell numbers did not contribute significantly to postischemic changes in the INL and ONL as assessed by using immunocytochemical markers for microglial and Müller cells. The time course of cell death determined by the TUNEL technique also differed markedly in the retinal layers being rapid and transient in the inner retina but delayed and prolonged in the ONL. PCNA immunoreactivity was undetectable in the normal retina, but was specifically induced in neurons of the inner retina within 1 h after reperfusion and was sustained for at least 4 weeks. We conclude that in contrast to photoreceptors in the ONL, a significant proportion of inner retinal neurons is resistant to ischemic insult induced by transiently increased intraocular pressure and that PCNA may possibly play a role in the selective postischemic survival of these cells.

Ganglion cells of the rat retina show osteopontin-like immunoreactivity.

Osteopontin (OPN) is a negatively charged, highly acidic glycosylated phosphoprotein that contains an GRGDS amino acid sequence, characteristic of proteins that bind to integrin receptors, thereby playing crucial roles in a number of physiological processes. This study was conducted to examine the expression of OPN in the rat retina by Northern blot analysis, Western blot analysis and immunocytochemistry. The expression of OPN was identified in the retina and OPN-like immunoreactivity was present in a number of ganglion cells. Thus, OPN appears to be important in the retinal homeostasis.

Morphology and synaptic connectivity of nitric oxide synthase-immunoreactive neurons in the guinea pig retina.

Immunocytochemical methods with an antiserum against neuronal nitric oxide synthase (NOS) were applied to identify the morphology and synaptic connectivity of NOS-like immunoreactive neurons in the guinea pig retina. In the present study, two types of amacrine cells were labeled with anti-NOS antisera. Type 1 cells had large somata located in the inner nuclear layer (INL) with long, sparsely branched processes ramifying mainly in stratum 3 of the inner plexiform layer (IPL). The somata of type 2 cells (smaller diameters) were located in the INL. Some displaced amacrine cells in the ganglion cell layer were labeled. The soma size of the displaced amacrine cells was similar to that of the type 2 amacrine cells. However, processes originating from type 2 amacrine cells and displaced amacrine cells stratified mainly in strata 1 and 5, respectively. Some cone bipolar cells were weakly NOS-immunoreactive. The synaptic connectivity of NOS-like immunoreactive amacrine cells was identified in the IPL by electron microscopy. NOS-labeled amacrine cell processes received synaptic input from other amacrine cell processes and bipolar cell axon terminals in all strata of the IPL. The most frequent postsynaptic targets of NOS-immunoreactive amacrine cells were other amacrine cell processes. Cone bipolar cells were postsynaptic to NOS-labeled amacrine cells in all strata of the IPL. Labeled amacrine cells synapsing onto ganglion cells were found only in sublamina b. A few synaptic contacts were observed between labeled cell processes. In the outer plexiform layer, dendrites of labeled bipolar cells made basal contact with cone pedicles or formed a synaptic triad opposed to a synaptic ribbon of cone pedicles.

Synaptic connectivity of two types of recoverin-labeled cone bipolar cells and glutamic acid decarboxylase immunoreactive amacrine cells in the inner plexiform layer of the rat retina.

We investigated the synaptic connectivity of two populations of recoverin-labeled bipolar cells and GABAergic neurons in the inner plexiform layer (IPL) of the rat retina. Two types of cone bipolar cells, type 2 and type 8, were stained with anti-recoverin antibodies, and GABAergic neurons were stained with anti-glutamic acid decarboxylase (GAD) antibodies. Type 2 cone bipolar axons received synaptic input from amacrine cell processes in 177 cases; among these amacrine cell processes, 92 processes (52.0%) were GAD-like immunoreactive. A total of 159 amacrine cell processes, which are presynaptic to type 8 cone bipolar cells, were observed. Among these processes, 117 processes (73.6%) were GAD-like immunoreactive. The postsynaptic elements at the ribbon synapses of recoverin-labeled cone bipolar cells were observed in 482 processes. In both type 2 and type 8 cone bipolar cells, the major output was to amacrine cell processes. At the ribbon synapses of the type 2 cone bipolar cells, 224 of the postsynaptic profiles were amacrine cell processes, 97 processes (43.3%) were GAD-like immunoreactive. In type 8 cone bipolar cells, 45 processes (30.2%) of 149 amacrine cell processes were GAD-like immunoreactive. Our results provide morphological evidence that GABA is a major transmitter involved in the visual processing of type 2 and 8 cone bipolar cells and GABA may have a stronger influence on type 8 cone bipolar cells than type 2 cone bipolar cells in the IPL of the rat retina.

Immunocytochemical localization of nitric oxide synthase in the mammalian retina.

The localization of nitric oxide synthase (NOS) was investigated by immunocytochemistry and immunoblotting using an antiserum against neuronal NOS in the rat, mouse, guinea pig, rabbit and cat retinae. Western blot analysis of retinal tissue extracts showed that the NOS-immunoreactive band of 155 kDa was present in all species. In the rat, mouse, guinea pig and rabbit retinae, two types of amacrine cells and a class of displaced amacrine cells were consistently NOS-labeled. In the cat retina, unlike other mammals, one type of amacrine cells and two types of displaced amacrine cells showed NOS immunoreactivity. NOS immunoreactivity was further found in some bipolar cells of the rat and guinea pig, some interplexiform cells of the mouse, some photoreceptor cells of the rabbit and some Müller cells of the cat.

Light and electron microscopical analysis of nitric oxide synthase-like immunoreactive neurons in the rat retina.

We have investigated the morphology of the NOS-like immunoreactive neurons and their synaptic connectivity in the rat retina by immunocytochemistry using antisera against nitric oxide synthase (NOS). In the present study, several types of amacrine cells were labeled with anti-NOS antisera. Type 1 cells had large somata located in the inner nuclear layer (INL) with long and sparsely branched processes ramifying mainly in stratum 3 of the inner plexiform layer (IPL). Somata of type 2 cells with smaller diameters were also located in the INL. Their fine processes branched mostly in stratum 3 of the IPL. A third population showing NOS-like immunoreactivity was a class of displaced amacrine cells in the ganglion cell layer (GCL). Their soma size was similar to that of the type 1 cells; however, their processes stratified mainly in strata 4 and 5 of the IPL. Labeled neurons were evenly distributed throughout the retina, and the mean densities were 57.0 +/- 9.7 cells/mm2 for the type 1 cells, 239.3 +/- 43.4 cells/mm2 for the type 2 cells and 121.2 +/- 27.5 cells/mm2 cells for the displaced amacrine cells. The synaptic connectivity of NOS-like immunoreactive amacrine cells was identified in the IPL by electron microscopy. NOS-labeled amacrine cell processes received synaptic input from other amacrine cell processes and bipolar cell axon terminals in all strata of the IPL. The most frequent postsynaptic targets of NOS-immunoreactive amacrine cells were other amacrine cell processes. Ganglion cell dendrites were also postsynaptic to NOS-like immunoreactive neurons in both sublaminae of the IPL. Synaptic outputs onto bipolar cells were observed in sublamina b of the IPL. In addition, a few synaptic contacts between labeled cell processes were observed. Our results suggest that NOS immunoreactive cells may be modulated by other amacrine cells and ON cone bipolar cells, and act preferentially on other amacrine cells.

Horizontal cells of the rat retina are resistant to degenerative processes induced by ischemia-reperfusion.

The fate of calbindin D28k (calbindin)-labeled horizontal cells in the ischemic rat retina induced by increasing intraocular pressure was investigated by immunocytochemistry using an antiserum against calbindin. In the normal retina, strong calbindin-like immunoreactivity was seen in the horizontal cells, and the density of the labelled horizontal cells was 815.3+/-15.2 per mm2. The thickness of the treated retina became progressively thinner with increasing reperfusion time after the ischemic insult due to a loss of retinal cells in the inner and outer nuclear layers. However, the densities of the horizontal cells per mm2 were 814.0+/-26.4 at 1 week, 813.3+/-20.8 at 2 weeks, and 812.6+/-11.5 at 4 weeks, indicating that horizontal cells did not degenerate during experimental periods. Thus, calbindin may have a protective role for horizontal cells to ischemic insult by its ability to buffer calcium influx in the rat retina.