Objective: Vascular Dementia (VaD), is associated with metabolic conditions. Diabetes is a major risk factor for the development of VaD. This study investigates the efficacy of ulinastatin (UTI) and sulforaphane (SUL) in streptozotocin (STZ)-diabetes induced vascular endothelium dysfunction and related dementia. Methods: Single dose STZ (50 mg/kg i.p.) was administered to Albino Wistar rats (male, 200−250 g). Morris water maze and attentional set shifting tests were used to assess the spatial learning, memory, reversal learning, and executive functioning in animals. Body weight, serum glucose, serum nitriteitrate, vascular endothelial function, aortic superoxide anion, brains’ oxidative markers (thiobarbituric acid reactive species-TBARS, reduced glutathione-GSH, superoxide dismutase-SOD, and catalase-CAT), inflammatory markers (IL-6, IL-10, TNF-, and myeloperoxidase-MPO), acetylcholinesterase activity-AChE, blood brain barrier (BBB) permeability and histopathological changes were also assessed. UTI (10,000 U/kg) and SUL (25 mg/kg) were used alone as well as in combination, as the treatment drugs. Donepezil (0.5 mg/kg) was used as a positive control. Results: STZ-administered rats showed reduction in body weight, learning, memory, reversal learning, executive functioning, impairment in endothelial function, BBB permeability, increase in serum glucose, brains’ oxidative stress, inflammation, AChE-activity, BBB permeability and histopathological changes. Administration of UTI and SUL alone as well as in combination, significantly and dose dependently attenuated the STZ-diabetes-induced impairments in the behavioral, endothelial, and biochemical parameters. Conclusion STZ administration caused diabetes and VaD which was attenuated by the administration of UTI and SUL.Therefore, these agents may be studied further for the assessment of their full potential in diabetes induced VaD.

Objective: Vascular Dementia (VaD), is associated with metabolic conditions. Diabetes is a major risk factor for the development of VaD. This study investigates the efficacy of ulinastatin (UTI) and sulforaphane (SUL) in streptozotocin (STZ)-diabetes induced vascular endothelium dysfunction and related dementia. Methods: Single dose STZ (50 mg/kg i.p.) was administered to Albino Wistar rats (male, 200−250 g). Morris water maze and attentional set shifting tests were used to assess the spatial learning, memory, reversal learning, and executive functioning in animals. Body weight, serum glucose, serum nitriteitrate, vascular endothelial function, aortic superoxide anion, brains’ oxidative markers (thiobarbituric acid reactive species-TBARS, reduced glutathione-GSH, superoxide dismutase-SOD, and catalase-CAT), inflammatory markers (IL-6, IL-10, TNF-, and myeloperoxidase-MPO), acetylcholinesterase activity-AChE, blood brain barrier (BBB) permeability and histopathological changes were also assessed. UTI (10,000 U/kg) and SUL (25 mg/kg) were used alone as well as in combination, as the treatment drugs. Donepezil (0.5 mg/kg) was used as a positive control. Results: STZ-administered rats showed reduction in body weight, learning, memory, reversal learning, executive functioning, impairment in endothelial function, BBB permeability, increase in serum glucose, brains’ oxidative stress, inflammation, AChE-activity, BBB permeability and histopathological changes. Administration of UTI and SUL alone as well as in combination, significantly and dose dependently attenuated the STZ-diabetes-induced impairments in the behavioral, endothelial, and biochemical parameters. Conclusion STZ administration caused diabetes and VaD which was attenuated by the administration of UTI and SUL.Therefore, these agents may be studied further for the assessment of their full potential in diabetes induced VaD.

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.The current study has utilized brivaracetam (BRV), a synaptic vesicle protein 2A modulator in experimental model of CI/R injury. Methods: CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory, motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor-α and interleukin-10), and acetylcholinesterase activity (AChE) in brain supernatants. Results: CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. Conclusion It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.The current study has utilized brivaracetam (BRV), a synaptic vesicle protein 2A modulator in experimental model of CI/R injury. Methods: CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory, motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor-α and interleukin-10), and acetylcholinesterase activity (AChE) in brain supernatants. Results: CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. Conclusion It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.The current study has utilized brivaracetam (BRV), a synaptic vesicle protein 2A modulator in experimental model of CI/R injury. Methods: CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory, motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor-α and interleukin-10), and acetylcholinesterase activity (AChE) in brain supernatants. Results: CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. Conclusion It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.The current study has utilized brivaracetam (BRV), a synaptic vesicle protein 2A modulator in experimental model of CI/R injury. Methods: CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory, motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor-α and interleukin-10), and acetylcholinesterase activity (AChE) in brain supernatants. Results: CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. Conclusion It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.

INTRODUCTIONKnowledge of morphological variations of the suprascapular region is important in the management of entrapment neuropathy and interventional procedures. The objective of this study was to collect data on the morphological features and dimensions of ossified ligaments and unusual bony tunnels of scapulae from a North Indian population.

METHODSA total of 268 adult human scapulae of unknown gender were obtained from the bone bank of the Department of Anatomy, Dayanand Medical College and Hospital, Ludhiana, Punjab, India. The scapulae were evaluated for the incidence of ossified superior transverse scapular ligaments (STSLs), ossified inferior transverse scapular ligaments (ITSLs) and bony tunnels (i.e. the bony canal between the suprascapular notch and spinoglenoid notch), found along the course of the suprascapular nerve (SSN). The dimensions of these structures were measured and noted down. Ossified STSLs were classified based on their shape (i.e. fan- or band-shaped) and the dimensions of the ossified suprascapular openings (SSOs) were measured.

RESULTSOssified STSLs were present in 26 (9.7%) scapulae. Among the 26 scapulae, 16 (61.5%) were fan-shaped (mean area of SSO 16.6 mm(2)) and 10 (38.5%) were band-shaped (mean area of SSO 34.2 mm(2)). Bony tunnels were observed in 2 (0.75%) specimens, while an ossified ITSL was observed in 1 (0.37%) specimen.

CONCLUSIONThe data obtained in the present study augments the reference literature for SSN decompression and the existing anatomical databases, especially those on Indian populations. This data is useful to clinicians, radiologists and orthopaedic surgeons.

Adult ; Cadaver ; Humans ; Ligaments, Articular ; anatomy & histology ; Nerve Compression Syndromes ; diagnosis ; epidemiology ; Ossification, Heterotopic ; diagnosis ; epidemiology ; Scapula ; anatomy & histology

INTRODUCTIONDetailed anatomical knowledge of the suprascapular notch (SSN) is important for the management of entrapment neuropathy and interventional procedures. The objective of the present study was to collect data on the morphological features and anatomical variations of the SSN in an Indian population.

METHODSWe studied 268 human scapulae of unknown sex (126 right-sided, 142 left-sided) taken from the Department of Anatomy, Dayanand Medical College and Hospital, India. SSNs were classified as either type I, II, III, IV or V, based on the shape of the inferior border of the incisura, and comparison of the SSN's vertical and transverse diameters. The shape of the SSN (i.e V- or U-shaped), if present, was also recorded.

RESULTSType II SSN was the most common (50.00%), followed by type I, type IV and type III (32.46%, 9.70% and 7.84%, respectively). For right-sided type II SSNs, the transverse and vertical diameters were 9.1 ± 3.2 mm and 5.2 ± 1.9 mm, respectively, while those for left-sided type ll SSNs were 9.2 ± 2.4 mm and 5.1 ± 1.8 mm, respectively. Generally, the transverse diameter of type II SSN was found to be greater than that of type III SSN. The incidence of U-shaped SSN was 51.49%, while that of V-shaped SSN was 2.99%.

CONCLUSIONThis study of the morphometrical characteristics and anatomical variations of SSN provides an anatomical database of SSN in the Indian context. This database will be of use in surgical procedures, as the information can be used to ensure adequate access to and complete decompression of the suprascapular nerve.

Humans ; India ; Nerve Compression Syndromes ; diagnosis ; Scapula ; anatomy & histology ; surgery ; Shoulder Joint ; injuries