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Analyzing abdominal muscles and measuring useful associated morphological features is important in many clinical researches. While ultrasonography is a non-invasive reliable tool for such tasks, it may cause the experimenter dependent subjective diagnosis thus a computer vision based automatic muscle detector/analyzer is much needed in this area. In this paper, we propose such an automatic vision based method using a series of image processing algorithms. The novelty of our method is to extract internal oblique muscle from abdominal ultrasonographic image which was excluded in previous study due to their irregular features. Previously, we used Mask searching method to restore vague part of abdominal image but the third layer of muscle (transverse abdominis) was not clearly extracted because of the image distortion in the process. In order to analyze muscle morphometric features like the thickness, the second layer (internal oblique muscle) should also be extracted correctly thus we develop a new muscle extraction process that includes extracting the second layer by using unsharp masking. Extraction of transverse abdominis is also improved by developing a new data structure Both-Map in candidate search process. In that process, we save the morphological features of initially extracted muscle area and later such information is used to restore the fascia area with various image processing techniques to extract target muscle accurately. The effectiveness of the proposed method is verified by the practical diagnostic field of rehabilitation in the extraction accuracy and the magnitude of the muscle thickness measurement error that lies within 0.02cm in more than 60% of cases used in the experiment.

Influenza is a seasonal disease that peaks every year in the winter months. Antigenic drift of the viral surface proteins, particularly the hemagglutinin (HA), is responsible for the virus's ability to evading the host's immune system, and for the severity of the disease. Pandemic influenza arises when an influenza virus carrying a novel HA gene enters into the naive human population, resulting in excess morbidity and mortality. Three major influenza pandemics were experienced in the last century and the emergence of a new pandemic strain is considered a matter of time. Our current understanding suggests that pandemic influenza strains arise from influenza viruses circulating in the natural reservoir, although the presence of intermediate hosts is considered essential in this process. Pigs and land-based birds have been shown to play a major role in the ecology of influenza viruses by providing an environment in which influenza viruses can change their phenotype, expand their host range, and eventually transmit to humans. In recent years, a great detail of attention has been placed on understanding the epidemiological and molecular factors that can lead to interspecies transmission of influenza viruses. In this review we will discuss the ecological and molecular aspects that lead to pandemic influenza as well as the intervention strategies at our disposal that can reduce the emergence of pandemic influenza strains and/or minimize their effects.

The calcium channel alpha2delta-1 subunit is a structural subunit important for functional calcium channel assembly. In vitro studies have shown that this subunit is the binding site for gabapentin, an anticonvulsant that exerts antihyperalgesic effects by unknown mechanisms. Increased expression of this subunit in the spinal cord and dorsal root ganglia (DRG) has been suggested to play a role in enhanced nociceptive responses of spinal nerve-injured rats to innocuous mechanical stimulation (allodynia). To investigate whether a common mechanism underlies allodynic states derived from different etiologies, and if so, whether similar alpha2delta-1 subunit up-regulation correlates with these allodynic states, we compared DRG and spinal cord alpha2delta-1 subunit levels and gabapentin sensitivity in allodynic rats with mechanical nerve injuries (sciatic nerve chronic constriction injury, spinal nerve transection, or ligation), a metabolic disorder (diabetes), or chemical neuropathy (vincristine neurotoxicity). Our data indicated that even though allodynia occurred in all types of nerve injury investigated, DRG and/or spinal cord alpha2delta-1 subunit up-regulation and gabapentin sensitivity only coexisted in the mechanical and diabetic neuropathies. Thus, induction of the alpha2delta-1 subunit in the DRG and spinal cord is likely regulated by factors that are specific for individual neuropathies and may contribute to gabapentin-sensitive allodynia. However, the calcium channel alpha2delta-1 subunit is not the sole molecular change that uniformly characterizes the neuropathic pain states.

Recent studies have suggested that cell migratory responses are often mediated by G(i) protein-coupled receptors. Because it is known that CB1 cannabinoid receptors are coupled to pertussis toxin-sensitive G proteins, we proposed that CB1 may mediate cell migration. To test this hypothesis, modified Boyden chamber assays were used to investigate cell migration mediated by CB1 cannabinoid receptors. HU-210, WIN55212-2, and anandamide, three cannabinoid agonists with distinct chemical structures, induced migration of human embryonic kidney 293 cells stably transfected with human CB1 gene, but not 293 cells transfected with an empty expression vector. These migratory responses were concentration-dependent. The EC(50) values for HU-210, WIN55212-2, and anandamide were 0.19 +/- 0.04, 12. 2 +/- 1.4, and 39.9 +/- 3.7 nM, respectively. The maximal migration index for HU-210, WIN55212-2, and anandamide were 8.9 +/- 1.6, 9.5 +/- 1.6, and 8.8 +/- 1.3, respectively. Pretreating cells with 100 ng/ml pertussis toxin eliminated the cannabinoid agonist-induced cell migration. SR141716A, a selective antagonist for CB1, inhibited the cannabinoid agonist-induced migratory responses in a concentration-dependent manner. Checkerboard analysis demonstrated that anandamide-induced cell migrations are due to chemotaxis as well as chemokinesis. Furthermore, anandamide-induced migratory responses were inhibited, in a concentration-dependent manner, by PD098059, an inhibitor of mitogen-activated protein kinase activation, but not by 8-bromoadenosine-3',5'-cyclic monophosphate, a cell-permeable cAMP analog. These data demonstrate that cannabinoid agonists are able to induce chemotaxis and chemokinesis, and that these migratory responses are mediated by G protein-coupled, CB1 cannabinoid receptors. In addition, these data suggest that activation of mitogen-activated protein kinase plays an important role, whereas inhibition of adenylate cyclase is probably not involved in the cell migration mediated by CB1.

It is known that marijuana smoking and administration of natural cannabinoids reduce intraocular pressure. However, it has not been established whether the intraocular pressure-lowering effects of cannabinoids are mediated by cannabinoid receptors. Aminoalkylindoles are a new class of cannabimimetics with structures entirely different from those of natural cannabinoids. WIN55212-2, a prototypic aminoalkylindole, has been shown to bind cannabinoid receptors and to exhibit cannabinoid-like activities. The objective of this study was to determine whether aminoalkylindoles lower intraocular pressure and whether the effects of aminoalkylindoles are mediated by ocular cannabinoid receptors. The intraocular pressure of New Zealand White rabbits was measured with the use of applanation pneumatonography. After the measurement of baseline intraocular pressure, drugs were applied topically and the intraocular pressure was monitored. The topical application of WIN55212-2 significantly reduced intraocular pressure in the treated eyes. The intraocular pressure-lowering effects of WIN55212-2 were time and dose dependent, and the maximal reduction was 4.7 +/- 0.5 mm Hg at a dose of 100 microg. In contrast to treated eyes, the intraocular pressure on the contralateral eyes was not significantly affected. The topical application of WIN55212-3, the enantiomer of WIN55212-2, had no effect on intraocular pressure. Furthermore, the intraocular pressure-lowering effects of WIN55212-2 were significantly reduced by topically administered SR141716A, a selective antagonist for the CB1 cannabinoid receptor. The dose-response curve of WIN55212-2 is shifted parallel to the right by SR141716A. These data demonstrate that like natural cannabinoids, WIN55212-2 also reduces intraocular pressure, and the effects of WIN55212-2 are mediated at least in part by the CB1 cannabinoid receptors in the eye.

Identified in December 2019, SARS-CoV-2 quickly spread worldwide with a resultant increase in global morbidity, mortality, and economic disruption on a scale not seen since the 1918 Spanish flu. Health officials recommended universal masking to further reduce human-to-human spread of SARS-CoV-2. The state of Hawaii and the Department of Defense (DOD) adopted strict mask policies early in the pandemic and is shown to be effective at reducing transmission. We report a case of Staphylococcus aureus bacteremia in an immunocompetent 21-year-old man attributed to local skin irritation with resultant infection in the setting of continuous reuse of a mask that resulted in bilateral cavernous venous thrombosis and septic pulmonary embolism.

It has been reported that WIN55212-2, a prototypic aminoalkylindole, has higher affinity for CB(2) than for CB(1). To explain the selectivity of WIN55212-2 for CB(2), molecular modeling studies were performed to probe the interacting sites between WIN55212-2 and cannabinoid receptors. In TMH5 the position 5.46 is a Phe in CB(2) versus a Val in CB(1). Docking of WIN55212-2 into the models of CB(1) and CB(2) predicts that F5.46 will result in a greater aromatic stacking of CB(2) with WIN55212-2. Using site-directed mutagenesis, this hypothesis was tested by exchanging the amino acids at position 5.46 between CB(1) and CB(2). Two mutations, including a Phe to Val mutation at the position 5.46 in CB(2) (CB2F5. 46V), and a corresponding Val to Phe mutation at the position 5.46 in CB(1) (CB(1)V5.46F), were made. The mutant receptors were transfected into 293 cells, and stable cell lines expressing similar numbers of receptors as wild-type receptors were chosen for additional ligand binding and cAMP accumulation studies. In ligand- binding assays, the CB(2)F5.46V mutation decreased the affinity of WIN55212-2 for CB(2) by 14-fold. In contrast, the CB(1)V5.46F mutation increased the affinity of WIN55212-2 for CB(1) by 12-fold. However, these mutations did not change the affinity of HU-210, CP-55940, and anandamide for CB(1) and CB(2). In cAMP accumulation assays, the changes in EC(50) values of WIN55212-2 were consistent with the changes in its binding affinity caused by the mutations. These results strongly support the hypothesis that the selectivity of WIN55212-2 for CB(2) over CB(1) is attributable to the change from Val in CB(1) at position 5.46 to Phe in CB(2).

Nitromethylene heterocycle insecticides are known to act on the nicotinic acetylcholine receptor-channel. The effects of the nitromethylene heterocycle, imidacloprid, on the nicotinic acetylcholine receptor-channel of clonal rat phaeochromocytoma (PC12) cells were studied using whole-cell and single-channel patch clamp methods. Imidacloprid suppressed carbachol-induced whole-cell currents in a dose-dependent manner, and this compound itself generated small currents. Multiple conductance states of single-channel currents were also evoked by imidacloprid at the nicotinic acetylcholine receptor-channels. The most frequently generated single-channel currents showed two conductance states, 25.4 and 9.8 pS, which were identical to the conductance states of acetylcholine-generated currents. The mean open time and burst duration of the main conductance currents induced by imidacloprid were shorter than those induced by acetylcholine. Co-application of imidacloprid and acetylcholine caused some interactions at the two conductance states. Mean open time and mean burst duration of the main conductance state currents evoked by acetylcholine were decreased by the co-application of imidacloprid as compared with those induced by acetylcholine alone. In conclusion, imidacloprid has both multiple agonist and antagonist effects on the neuronal nicotinic acetylcholine receptor-channels.

The effects of riluzole, a neuroprotective drug, on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neurons were studied using the whole-cell patch-clamp technique. Riluzole inhibited HVA calcium channel currents in a dose-dependent, time-dependent and reversible manner. The apparent dissociation constants for riluzole inhibition of the transient and sustained components of the current were 42.6 and 39.5 microM, respectively. Riluzole accelerated the activation kinetics of calcium channels without affecting the voltage dependence of activation. It accelerated the fast component of deactivation kinetics without affecting the slow component. It also accelerated fast and slow inactivation kinetics of the HVA channels. However, only one of the two components in the steady-state inactivation curve for the HVA channels was shifted in the hyperpolarizing direction by riluzole, which indicates differential block of the multiple-type HVA channels. By use of the specific blockers nimodipine, omega-conotoxin GVIA and omega-agatoxin IVA, the HVA calcium channels were found to comprise L-type (10%), N-type (63%), P/Q-type (23%) and R-type (9%). Riluzole blocked N- and P/Q-type channels, but not L-type channel, with the order of efficacy of P/Q- > N- >> L-type channels. Riluzole inhibition of N- and P/Q-type calcium channels may result in reduced calcium influx at presynaptic terminals, which thereby decreases excessive excitatory neurotransmitter release, especially glutamate, a mechanism known to cause neuronal death in ischemic conditions.

The effects of riluzole, a neuroprotective drug, on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in rat dorsal root ganglion neurons were studied using the whole-cell patch clamp technique. At the resting potential, riluzole preferentially blocked TTX-S sodium channels, whereas at more negative potentials, it blocked both types of sodium channels almost equally. The apparent dissociation constants for riluzole to block TTX-S and TTX-R sodium channels in their resting state were 90 and 143 microM, respectively. Riluzole shifted the voltage dependence of activation of TTX-R sodium channels in the depolarizing direction more than that of TTX-S sodium channels. The voltage dependence of the fast inactivation of both types of sodium channels was shifted in the hyperpolarizing direction in a dose-dependent manner, and the apparent dissociation constants for riluzole to block the inactivated channels were estimated to be 2 and 3 microM for the TTX-S and TTX-R sodium channels, respectively, indicating a much higher affinity for the inactivated channels than for the resting channels. Riluzole was equally effective in blocking both types of sodium channels in their slow inactivated state. Since more TTX-S channels are inactivated than TTX-R channels at the resting potential, riluzole blocks TTX-S sodium channels more potently than TTX-R sodium channels. It was concluded that one of the mechanisms by which riluzole exerts its neuroprotective action is to preferentially block the inactivated sodium channel of damaged or depolarized neurons under ischemic conditions, thereby suppressing excess stimulation of the glutamatergic receptors and massive influx of Ca++.

Sugammadex hypersensitivity is an uncommon event that typically occurs at higher doses. We report a case of suspected sugammadex hypersensitivity in a patient who developed hypoxia and bronchospasm following three administrations of the standard 2 mg/kg doses of sugammadex within 26 hours due to flap takebacks. Hypersensitivity to sugammadex was not initially suspected given that the patient had previous exposures. Diagnoses of pneumothorax, hemothorax, mucus plug, and tracheal tube malposition were immediately ruled out. Furthermore, the onset of hypoxia with sudden loss of tidal volume, development of high peak airway pressures, and temporal correlation with sugammadex administration all supported bronchospasm secondary to a hypersensitivity reaction. Sugammadex is a useful agent for neuromuscular blockade reversal; however, it is critical to carefully examine all adverse reactions. This case report highlights the importance of considering hypersensitivity reactions in the setting of repeat sugammadex administrations in a limited timeframe, such as in free flap reconstruction requiring multiple takebacks to the operating room in the setting of flap compromise.