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Prostatic adenocarcinoma is the most common type of cancer in men, with subsequent lesions most commonly occurring in the lymph nodes, bones, and lungs.1,2 We discuss the clinical case of a 59-year-old man who presented after radical prostatectomy for prostate cancer with a unilateral metastasis in the right testis. Metastases to the testis are uncommon, occurring in less than 4% of cases.2,3 This kind of metastasis is usually unilateral, manifesting as a palpable testicular mass, and rarely involves both the testis and the epididymis.1,2 Secondary neoplasms of the testis are found in around 2.5% of autopsies, including nonneoplastic fatalities.2 Most secondary testicular metastases develop from distant primary locations, the most prevalent of which are the lung, prostate, and gastrointestinal tract.2 Testicular metastases can occur in up to 4% of all prostate cancer cases and are frequently discovered by chance following orchiectomy therapy for advanced disease.4 In general, advanced prostate cancer metastases to the pelvic lymph nodes, bones, lungs, and liver are common; however, few of these patients have clinically evident testicular metastasis.4,5 Secondary neoplasms of the testis are uncommon, with a reported rate of 0.02-2.5%, except leukemia and lymphoma infiltration.2,3 The prostate is the most common site of testicular metastases (15%), followed by the lung, melanomas, skin, colon, and kidney.1,2 However, most testicular metastases of prostate cancer were discovered after examining a significant number of testes from patients who had tumors removed during therapeutic orchiectomies.2,4 Lung cancer (43%), malignant melanoma (20%), pancreatic cancer (10%), and prostate cancer (10%) are among cancers that can spread to the testes.4,5 However, the great majority of metastases are lesions detected by chance following an autopsy or bilateral orchiectomy for Prostatic Cancer hormonal treatment.3 A testicular tumor revealing clinical recurrence is highly unusual. Bubendorf et al.1 discovered testicular metastases in just 0.5% of 1,589 prostate carcinoma autopsy reports. He also suggests a backward metastatic channel through prostate veins in addition to the typical hematogenous tumor spread via the vena cava. Overall, four routes have been hypothesized for the propagation of the lesions to the testis: retrograde venous extension, retrograde lymphatic extension, arterial embolism, and through the lumen of the vas deferens.1 Patients with symptomatic isolated post-prostatectomy testicular metastases can live for a surprisingly long time after orchidectomy without further development. This phenomenon may be linked to cytoreduction.1,2 The ability to manage the malignant process locally is an undeniable clinical benefit for patients undergoing orchiectomy. Given that this method of treatment is easy, safe, and associated with few problems, all patients with isolated prostatic cancer testicular metastases should be considered candidates for metastasectomy.4,5 The histological features of prostate cancer testicular metastases are similar to those of original prostate tumors; however, histology may show a more aggressive phenotype with a significant probability of future disease spreading and, thus, worse survival.3,4 Weitzner4 found that patients with newly diagnosed testicular metastases from prostate cancer had a median survival of roughly 12 months.1,2 Other studies, on the other hand, have documented survival of more than two years without biochemical relapses. As a result, the predictive impact of testicular metastases from prostate cancer is yet unknown, owing to the rarity of the incidence.2 Testicular metastasis from prostate carcinoma is an uncommon manifestation of advanced disease.2 It often presents with testicular pain, swelling, or a palpable mass and can mimic primary testicular neoplasms. Clinicians should maintain a high index of suspicion, especially in patients with a history of prostate carcinoma. Prompt diagnosis through imaging studies and histopathological confirmation is essential for appropriate management and prognosis.3,4 This case underscores the importance of considering testicular metastasis in the differential diagnosis of testicular masses, particularly in patients with a history of prostate carcinoma. A multidisciplinary approach is crucial for optimal management and improving patient outcomes. Early recognition and timely intervention are paramount in managing metastatic disease and improving quality of life. Figure 1 refers to a 59-year-old male patient presented to our hospital with an elevated serum prostate-specific antigen (PSA) level of >100 ng/ml. He had been on regular follow-up with urology for surveillance of prostate cancer recurrence. He had undergone a radical prostatectomy two years ago with Gleason grade group 5. Scrotal ultrasound showed a hypoechoic mass involving the right testicle with increased vascularity, suggesting a neoplastic lesion. Hence, the patient was planned for a bilateral orchidectomy. The patient underwent bilateral inguinal orchiectomy without any complications. Macroscopic examination of the right resected testis revealed a solid yellowish-white tumor of 0.5 × 0.5 cm. Histopathological analysis showed that the right testis was infiltrated by metastatic adenocarcinoma. Immunohistochemical examination revealed that tumor cells were diffusely positive for PSA and Alpha (α)-methylacyl-CoA racemase (AMACR). The patient was diagnosed with right testicular metastasis of Prostatic Carcinoma. The patient had an uneventful postoperative recovery. The patient was scheduled for regular follow-up appointments to monitor disease progression. Serial PSA levels and imaging studies were planned to look for disease status. Figure 1 A – Gross view of the right orchidectomy showing a small nodular metastatic deposit in tunica albuginea from the prostate cancer; B, C and D are photomicrographs of the tumor and testicle parenchyma; B – shows normal testicular seminiferous tubules along with presence of metastatic tumor deposit in the wall of testis (Tunica albuginea) (H&E x100); C – These tumor cells are immunopositive for prostate specific antigen (PSA 40X); D – The tumor cells are also positive for Alpha-methylacyl-CoA racemase (AMACR 200X).:

In India, the incidence of mucormycosis reached high levels during 2021–2022, coinciding with the COVID-19 pandemic. In response to this, we established a multicentric ambispective cohort of patients hospitalised with mucormycosis across India. In this paper, we report their baseline profile, clinical characteristics and outcomes at discharge. Patients hospitalized for mucormycosis during March–July 2021 were included. Mucormycosis was diagnosed based on mycological confirmation on direct microscopy (KOH/Calcofluor white stain), culture, histopathology, or supportive evidence from endoscopy or imaging. After consent, trained data collectors used medical records and telephonic interviews to capture data in a pre-tested structured questionnaire. At baseline, we recruited 686 patients from 26 study hospitals, of whom 72.3% were males, 78% had a prior history of diabetes, 53.2% had a history of corticosteroid treatment, and 80% were associated with COVID-19. Pain, numbness or swelling of the face were the commonest symptoms (73.3%). Liposomal Amphotericin B was the commonest drug formulation used (67.1%), and endoscopic sinus surgery was the most common surgical procedure (73.6%). At discharge, the disease was stable in 43.3%, in regression for 29.9% but 9.6% died during hospitalization. Among survivors, commonly reported disabilities included facial disfigurement (18.4%) and difficulties in chewing/swallowing (17.8%). Though the risk of mortality was only 1 in 10, the disability due to the disease was very high. This cohort study could enhance our understanding of the disease’s clinical progression and help frame standard treatment guidelines.

This paper demonstrates a low-profile, wide-band, two-element, frequency-reconfigurable MIMO antenna that is suitable for diverse wireless applications of 4G and 5G such as WLAN/Bluetooth (2.4–2.5 GHz), WLAN (2.4–2.484 GHz, 5.15– 5.35 GHz, and 5.725–5.825 GHz), WiMAX (3.3–3.69 GHz and 5.25–5.85 GHz), Sub6GHz band proposed for 5G (3.4–3.6 GHz, 3.6-3.8GHz and 4.4–4.99 GHz), INSAT and satellite X-band(6 to 9.6 GHz). Proposed MIMO favour effortless switching between multiple bands ranging from 2.2 to 9.4 GHz without causing any interference. Both antenna elements in a MIMO array are made up of a single module comprised of a slot-loaded patch and a defective structured ground. Two PIN diodes are placed in the preset position of the ground defect to achieve frequencyreconfigurable qualities. The suggested MIMO antenna has a size of 62 ×25 ×1.5 mm3. Previous reconfigurable MIMO designs improved isolation using a meander line resonator, faulty ground structures, or self-isolation approaches. To attain the isolation requirements of modern devices, stub approach is introduced in proposed design. Without use of stub, simulated isolation is 15dB. The addition of a stub improved isolation even more. At six resonances, measured isolation is greater than 18 dB, the computed correlation coefficient is below 0.0065, and diversity gain is over 9.8 dB.

Abstract Individuals with Autism Spectrum Disorder (ASD; autism) commonly present with gastrointestinal (GI) illness in addition to core diagnostic behavioural traits. The appendix, or cecum in mice, is important for GI homeostasis via its function as a key site for fermentation and a microbial reservoir. Even so, the role of the appendix and cecum in autism-associated GI symptoms remains uninvestigated. Here, we studied mice with an autism-associated missense mutation in the post-synaptic protein neuroligin-3 (Nlgn3 R451C ), which impacts brain and enteric neuronal activity. We assessed for changes in cecal motility using a tri-cannulation video-imaging approach in ex vivo preparations from wild-type and Nlgn3 R451C mice. We investigated cecal permeability and neurally-evoked secretion in wild-type and Nlgn3 R451C tissues using an Ussing chamber set-up. The number of cecal patches in fresh tissue samples were assessed and key immune populations including gut macrophages and dendritic cells were visualised using immunofluorescence. Nlgn3 R451C mice displayed accelerated cecal motor complexes and reduced cecal weight in comparison to wildtype littermates. Nlgn3 R451C mice also demonstrated reduced neurally-evoked cecal secretion in response to the nicotinic acetylcholine receptor agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP), but permeability was unchanged. We observed an increase in the number of cecal patches in Nlgn3 R451C mice, however the cellular morphologies of key immune populations studied were not significantly altered. We show that the R451C nervous system mutation leads to cecal dysmotility, impaired secretion, and neuro-immune alterations. Together, these results suggest that the R451C mutation disrupts the gut-brain axis with GI dysfunction in autism.

Intestinal macrophages are well-studied for their conventional roles in the immune response against pathogens and protecting the gut from chronic inflammation. However, these macrophages may also have additional functional roles in gastrointestinal motility under typical conditions. This is likely to occur via both direct and indirect influences on gastrointestinal motility through interaction with myenteric neurons that contribute to the gut-brain axis, but this mechanism is yet to be properly characterised. The CX3CR1 chemokine receptor is expressed in the majority of intestinal macrophages, so we used a conditional knockout Cx3cr1-Dtr (diphtheria toxin receptor) rat model to transiently ablate these cells. We then utilized ex vivo video imaging to evaluate colonic motility. Our previous studies in brain suggested that Cx3cr1-expressing cells repopulate by 7 days after depletion in this model, so we performed our experiments at both the 48 hr (macrophage depletion) and 7-day (macrophage repopulation) time points. We also investigated whether inhibitory neuronal input driven by nitric oxide from the enteric nervous system is required for the regulation of colonic motility by intestinal macrophages. Our results demonstrated that CD163-positive resident intestinal macrophages are important in regulating colonic motility in the absence of this major inhibitory neuronal input. In addition, we show that intestinal macrophages are indispensable in maintaining a healthy intestinal structure. Our study provides a novel understanding of the interplay between the enteric nervous system and intestinal macrophages in colonic motility. We highlight intestinal macrophages as a potential therapeutic target for gastrointestinal motility disorders when inhibitory neuronal input is suppressed.